Endocrine Disruption

A robust and green CoAl-LDH@MoS2/glass TFME platform for highly sensitive determination of bisphenol a in aqueous matrices - June 1, 2026

Anal Chim Acta. 2026 Aug 22;1412:345617. doi: 10.1016/j.aca.2026.345617. Epub 2026 May 5.

ABSTRACT

BACKGROUND: Thin-film microextraction has emerged as a powerful solvent-free sample preparation technique, featuring a high surface area-to-volume ratio sorbent phase that enhances extraction efficiency and sensitivity compared to traditional approaches. ultraviolet detection; AGREEprep.

RESULTS: A novel thin-film microextraction platform based on cobalt-aluminum layered double hydroxide@ molybdenum disulfide grown on glass was developed for the efficient extraction of bisphenol A from aqueous matrices. The hierarchical heterostructure, prepared via a two-step hydrothermal method, combines molybdenum disulfide nanoflowers for π-π stacking with cobalt-aluminum layered double hydroxide nanopetals for hydrogen bonding and anion exchange, resulting in a high surface area (312 m² g^-1) and multimodal adsorption.

SIGNIFICANCE: The glass-supported film offers excellent stability (>100 reuse cycles) and thermal robustness (>620 °C decomposition). Optimized conditions include 8 min extraction at 200 rpm and desorption with 200 μL methanol. The method provides linearity from 0.01 to 100 μg L^-1, limit of detection 3.1 ng L^-1, limit of quantification 9.6 ng L^-1, enrichment factor 170, and relative standard deviation < 3.2% (repeatability, n = 3) across low (near limit of quantification), middle, and high calibration levels (inter-day RSD <8.6%). Real-sample relative recoveries ranged from 98% to 120% in thermal paper, mineral water, and tap water, with negligible matrix effects. The method scores 0.68 on AGREEprep, outperforming dispersive liquid-liquid microextraction (0.42), solid-phase microextraction (0.68), and hollow-fiber liquid-phase microextraction (0.51). This reusable, low-solvent platform is a sustainable option for endocrine disruptor monitoring, with potential for similar phenolic compounds.

PMID:42219632 | DOI:10.1016/j.aca.2026.345617

KNDy kisspeptin is required for metabolic homeostasis in female mice in an ovarian hormone-independent manner - June 1, 2026

J Neuroendocrinol. 2026 Jun;38(6):e70208. doi: 10.1111/jne.70208.

ABSTRACT

Disorders of gonadotropin pulsatility contribute to reproductive dysfunction in humans and are often associated with metabolic dysfunction. Hypogonadotropic hypogonadism is characterized by chronically insufficient gonadotropin hormone production, leading to reproductive and metabolic impairments, such as infertility and obesity. Polycystic ovary syndrome (PCOS) is characterized by accelerated gonadotropin hormone production leading to reproductive and metabolic deficits, including oligomenorrhea, infertility, and an increased risk of type 2 diabetes mellitus. Hypothalamic kisspeptin is a key regulator of gonadotropin secretion, and disruptions in kisspeptin signaling result in abnormal gonadotropin pulsatility. Emerging evidence also implicates kisspeptin in energy metabolism. This study investigates the neuroendocrine mechanisms by which kisspeptin within KNDy neurons influences metabolic homeostasis. Using a Pdyn-Cre/Kiss1^fl/fl knock-out (Kiss1^Pdyn KO) mouse model, we combined diet-induced obesity, metabolic testing, and ovarian hormone depletion to assess the role of KNDy neuron kisspeptin in metabolic regulation and the interaction with sex steroids. Peripheral metabolism was more severely impacted in Kiss1^Pdyn KO females than in KO males, with greater reproductive deficits observed in females. Abnormal glucose metabolism was partly attributable to the lack of ovarian steroids. Our findings indicate that loss of KNDy neuron kisspeptin in females promotes obesity through reduced energy expenditure without altering feeding behavior. Furthermore, this study identifies a female-biased role for KNDy kisspeptin as a central integrator of reproductive and metabolic signals.

PMID:42219677 | DOI:10.1111/jne.70208

A Narrative Review of Zebrafish Models of Diabetes Mellitus - June 1, 2026

Cureus. 2026 Apr 29;18(4):e107992. doi: 10.7759/cureus.107992. eCollection 2026 Apr.

ABSTRACT

Diabetes mellitus is a major chronic metabolic disease characterized by persistent hyperglycemia resulting from impaired insulin secretion, impaired insulin action, or both, and is associated with microvascular and macrovascular complications. Although rodent models remain central to diabetes research, zebrafish (Danio rerio) have emerged as a powerful complementary vertebrate model because of their genetic and physiological conservation with humans, rapid development, optical transparency during early life stages, high fecundity, low maintenance cost, and suitability for high-throughput drug screening. Several reviews have addressed specific aspects of zebrafish diabetes research, but fewer provide an integrated comparison across the major genetic, chemical, and dietary models while also emphasizing translational relevance, model selection, and practical limitations. This narrative review, therefore, provides a comparative overview of the major zebrafish diabetes models and their principal applications. We group models into genetic models with predominant beta-cell dysfunction or insulin deficiency and those with predominant insulin resistance or type 2 diabetes-like metabolic dysfunction; chemical models including beta-cell-toxic agents such as streptozotocin and alloxan, as well as metabolically oriented glucose immersion and endocrine-disruptor exposures; and dietary models based on overfeeding and high-fat, high-glucose, or combined cholesterol-glucose regimens. Across these model classes, we compare induction strategy, principal phenotype, relevance to type 1 versus type 2 diabetes, strengths, limitations, and typical research applications in drug discovery, regeneration, pharmacogenomics, and studies of complications. We also emphasize that there is no universally accepted single diagnostic glycemic threshold for diabetes in zebrafish; instead, model validation usually relies on sustained elevation of glucose relative to controls together with functional or mechanistic readouts such as glucose tolerance, insulin signaling, beta-cell mass, and lipid-metabolic changes. Despite important physiological differences from mammals and the strong regenerative capacity of zebrafish, the model provides a scalable vertebrate platform for mechanistic and early translational diabetes research.

PMID:42220722 | PMC:PMC13222082 | DOI:10.7759/cureus.107992

Associations between food contaminants exposure and pubertal development at 10 and 13 years old - May 31, 2026

Environ Res. 2026 May 30:124905. doi: 10.1016/j.envres.2026.124905. Online ahead of print.

ABSTRACT

Endocrine-disrupting compounds, such as acrylamide (AA) and bisphenol A (BPA), are external substances usually found in air, water, food and other consumer products that may influence puberty timing. This study aims to assess the association of AA and BPA, individually and combined, on pubertal development in a sample of children and adolescents aged 4-13. Data from Generation XXI cohort was used(n=5279). Dietary information was gathered through food diaries. Dietary AA exposure was estimated by merging food consumption with occurrence data from EFSA's publication. BPA exposure was estimated using a random forest model that integrated food consumption data with urinary BPA. Pubertal development was assessed by trained professionals at 10- and 13-years using Tanner scale. Linear regression models tested the associations between exposure to food contaminants (individually and combined), and pubertal development. The median dietary exposure was higher in boys for both AA and BPA, decreasing with age. A negative association was found between individual AA exposure at 7-years (-0.007(95%CI:-0.013,-0.002)), 10-years (-0.006(95%CI:-0.010,-0.003)) and 13-years (-0.005(95%CI:-0.009,-0.001)) and the pubertal development global score in girls, and a positive association for individual AA exposure at 13-years (0.003(95%CI:0.001,0.007)) in boys. A significant positive association between BPA exposure at 10 and 13 years and a higher pubertal development global score was only found in boys. Testing combined exposure did not significantly change the results observed for individual exposure to each food contaminant. Childhood and adolescent exposure to AA and BPA was associated with impaired timing of puberty timing, representing a relevant public health concern.

PMID:42218933 | DOI:10.1016/j.envres.2026.124905

Inflammatory Cytokines Impair Glucagon Expression and Secretion in Pancreatic α-Cells - May 31, 2026

Diabetes Obes Metab. 2026 May 31. doi: 10.1111/dom.70921. Online ahead of print.

ABSTRACT

AIMS: Insulin resistance and obesity-associated inflammation are key drivers in the pathogenesis of Type 2 diabetes mellitus (T2DM). Whilst inflammatory cytokines are well known to impair β-cell function, their impact on pancreatic α-cells and glucagon (GCG) regulation remains poorly understood. In this study, we investigated the effects of the pro-inflammatory cytokines interleukin (IL)-1β, tumour necrosis factor (TNF)-α and interferon (IFN)-γ on GCG expression and secretion.

MATERIALS AND METHODS: The viability and endocrine function of α-cell line αTC1 and isolated islets were investigated by WST-1 assay, LDH assay, qRT-PCR, Western blot analysis and ELISA. The transcriptional activity of the GCG promoter was analysed by reporter gene assays. The cellular composition of isolated islets was assessed by immunohistochemistry.

RESULTS: We found that exposure of the α-cell line αTC1 to a mix of these cytokines activates cellular stress responses characterised by induction of the nuclear factor kappa-light-chain-enhancer of activated B-cells (NF-κB) pathway and the nuclear factor erythroid 2-related factor 2 (Nrf2) pathway. Moreover, cytokine treatment markedly reduced GCG gene expression and secretion through repression of GCG promoter activity. Mechanistically, this was associated with a disrupted transcriptional network. These findings were confirmed in isolated mouse islets, where cytokine exposure significantly reduced GCG expression and secretion in islets of both male and female donors.

CONCLUSIONS: Taken together, these findings indicate that inflammatory cytokines are potent modulators of α-cell function as well as GCG secretion and provide novel insights into inflammation-driven dysregulation of the endocrine function of pancreatic islets.

PMID:42219277 | DOI:10.1111/dom.70921

Environmental estrogens and animal reproductive health: mechanisms, biomarkers, and intervention approaches - May 31, 2026

J Anim Sci Biotechnol. 2026 Jun 1;17(1):106. doi: 10.1186/s40104-026-01427-6.

ABSTRACT

Environmental estrogens, a group of exogenous endocrine-active compounds, are frequently present in animal feed, water, and husbandry environments. These compounds, which include synthetic xenoestrogens, phytoestrogens, and metalloestrogens, can disrupt reproductive physiology and developmental processes in domestic animals. This review examines their effects on key reproductive outcomes such as folliculogenesis, spermatogenesis, gamete quality, and overall fertility. We discuss the underlying molecular mechanisms, focusing on hormone receptor signaling and epigenetic modifications, and highlight the particular relevance of low-dose and developmental stage-specific exposure in breeding populations. Additionally, potential mitigation approaches are outlined, including nutritional strategies, feed management, and genetic or biotechnological interventions aimed at preserving reproductive performance and animal health. This review elucidates the reproductive toxicological mechanisms of environmental estrogens and provides a scientific basis for developing effective prevention and mitigation strategies.

PMID:42219524 | DOI:10.1186/s40104-026-01427-6

Fluorinated Cobalt Sites Enable Solar-Enhanced Neutral Active Chlorine Electrosynthesis for In Situ Seawater Purification - May 30, 2026

Angew Chem Int Ed Engl. 2026 May 30:e9156528. doi: 10.1002/anie.9156528. Online ahead of print.

ABSTRACT

The electrocatalytic chlorine evolution reaction (ClER) provides a sustainable approach for converting abundant seawater chloride into highly reactive chlorine species for in situ marine purification. However, the practical implementation remains limited by the need for precious-metal-based electrodes to achieve high selectivity, while under neutral conditions, intense competition from the oxygen evolution reaction (OER) and severe anode dissolution compromise both efficiency and stability. Here, we demonstrate a solar-driven strategy employing surface-fluorinated cobalt hydroxide nanosheets (Co(OH)_xF_y) as an efficient, highly selective, and precious-metal-free catalyst for neutral-pH ClER. This catalyst enables rapid degradation of a broad spectrum of prevalent marine contaminants within seconds, including antibiotics, phenols, and endocrine disruptors. In situ surface-interrogation scanning electrochemical microscopy (SI-SECM) and scanning electrochemical cell microscopy (SECCM) combined with theoretical calculations reveal that surface fluorination optimizes the coordination and electronic structure of Co(III) active sites, significantly enhancing intrinsic activity and selectivity, particularly at edge regions. Furthermore, the catalyst uniquely leverages photo-activation to selectively amplify chlorine generation. Integrated into a membrane-free photoelectrochemical flow reactor, this approach achieves direct seawater purification with significantly reduced energy demand and carbon emissions, demonstrating compelling promise for scalable, environmentally benign marine water treatment.

PMID:42216833 | DOI:10.1002/anie.9156528

Bionic phase-transitioned alpha-lactalbumin coating for efficient separation of structurally similar environmental endocrine disruptors by open tubular capillary electrochromatography - May 30, 2026

J Chromatogr A. 2026 May 19;1783:467121. doi: 10.1016/j.chroma.2026.467121. Online ahead of print.

ABSTRACT

Environmental endocrine disruptors with estrogenic effects pose a significant threat to human health. However, many of these disruptors are homologues or isomers with similar structures, making them difficult to separate. Therefore, it is crucial to develop simple, rapid, and effective methods for their separation and detection. In this study, we developed a phase transition α-lactalbumin nanofilm (PTLA) using a fast phase transition preparation method. The nanofilm can stably adhere to various substrate surfaces and exhibits excellent stability under extreme conditions such as high-tack tape peeling, acid-alkali exposure, organic solvents, and high-pressure resistance. Its large specific surface area and abundant chemical groups enhance interactions with analytes. As a result, the PTLA-enhanced open tubular capillary electrochromatography (OT-CEC) achieved baseline separation of bisphenol homologs in 11 min and nitrophenol isomers in 7 min. Additionally, the PTLA-coated capillary demonstrated remarkable reusability, performing over 200 cycles with consistent peak shape and resolution. The relative standard deviations (RSDs) for intra-day, inter-day, and column-to-column repeatability were within 6.2%. Thus, PTLA coatings represent a significant advancement in separation science.

PMID:42217391 | DOI:10.1016/j.chroma.2026.467121

Phenolic acids in root exudates mediate laccase-induced formation of estrogen precipitation co-polymers - May 30, 2026

Ecotoxicol Environ Saf. 2026 May 30;319:120322. doi: 10.1016/j.ecoenv.2026.120322. Online ahead of print.

ABSTRACT

Endocrine-disrupting estrogens, such as 17β-estradiol (E2) and bisphenol A (BPA), are commonly found in agroecosystems, posing substantial risks to crop productivity and public health. While laccase-induced polymerization transfer is an effective strategy for estrogen remediation, the interactive effects of living crop root-released exudates (e.g., sugars, phenolic acids, amino acids) on this enzymatic process remain largely unclear. Here, we employed artificial root exudates (AREs) containing environmentally relevant concentrations of key components to systematically dissect the regulatory roles of distinct root-exuded fractions in laccase-induced estrogen conversion. Compared to the ARE-deficient group, phenolic and amino acids in AREs collectively suppressed laccase-induced estrogen self-polymerization. Notably, phenolic acids exerted a distinct, complementary effect by mediating radical-controlled C-C and C-O-C co-polymerization between estrogen molecules and ARE components, resulting in robust precipitation of co-polymeric products. These precipitation co-polymers were assembled from moieties containing phenolic -OH, -COOH, and aryl functional moieties, exhibiting high structural complexity, morphological diversity, and dense packing that endow them with unique physicochemical properties. Furthermore, we selected maize (Zea mays L.) as a model crop and experimentally demonstrated that laccase reduced the estrogen pollution risks in maize seedlings by catalyzing rapid pollutant polymerization in the rhizosphere solution, effectively blocking root uptake and subsequent translocation to above-ground shoot tissues. Relative to the laccase-free group, laccase treatment significantly reduced E2 levels in maize roots and shoots by 59.26% and 54.78%, respectively, following 5-day exposure to 20 μmol·L⁻¹ E2. These findings offer a robust enzyme-induced polymerization way for mitigating estrogen pollution in agroecosystems, with critical implications for ensuring crop safety and agricultural sustainability.

PMID:42217488 | DOI:10.1016/j.ecoenv.2026.120322

Adolescent Ethanol Exposure Reprograms HMGB1 Responsivity to Adult Ethanol Challenge in Males - May 30, 2026

Physiol Behav. 2026 May 29:115404. doi: 10.1016/j.physbeh.2026.115404. Online ahead of print.

ABSTRACT

Adolescent intermittent ethanol (AIE) - a model of human adolescent binge drinking - produces lasting changes in ethanol responsivity, including increased adult ethanol consumption and behavioral tolerance. However, the neuroimmune and neuroplastic mechanisms underlying these adaptations are unclear. Therefore, we used a model of human adolescent binge drinking (AIE; 5 g/kg/day ethanol or water, i.g., 2-day on/2-day off cycle from postnatal day (PND) 25-54) to assess disruptions to immune, neuronal, and endocrine responsivity to an acute ethanol challenge (4 g/kg) in adulthood (PND 105-110) in male Wistar rats. Acute ethanol increased plasma HMGB1 in adult controls, whereas AIE blunted this response without altering baseline plasma HMGB1. In addition, AIE persistently elevated plasma ALT, indicating persistent hepatic injury. Ethanol-induced plasma corticosterone responses were intact, suggesting divergence in innate immune versus endocrine responses to a later ethanol challenge after AIE. In the brain, AIE produced region-specific alterations in HMGB1 immunoreactivity (IR), increasing HMGB1+IR in the dentate gyrus but reducing it in CA3 and CA1. An acute ethanol challenge decreased hippocampal HMGB1+IR in control animals only, suggesting AIE produces enduring tolerance to ethanol-induced HMGB1 cellular export in the hippocampal formation. AIE also increased cyclooxygenase-2 (COX-2)+IR in the dentate and basolateral amygdala (BLA), and HMGB1 and COX-2+IR correlated across subjects. In BLA, acute ethanol in adulthood increased COX-2 selectively in controls. Collectively, these data indicate that AIE produces enduring, region and molecular target-specific reprogramming of ethanol responsivity that differentially emerges across innate immune, neuronal, and endocrine domains.

PMID:42217537 | DOI:10.1016/j.physbeh.2026.115404

Tributyltin-dysregulated periprostatic adipose tissue enhances prostate cell survival and migration, implicating the C-C motif chemokine receptor 3 - May 30, 2026

J Environ Sci (China). 2026 Jul;165:225-238. doi: 10.1016/j.jes.2025.06.015. Epub 2025 Jun 9.

ABSTRACT

Obesity-dysregulated periprostatic adipose tissue (PPAT) has been implicated in the aggressiveness of prostate cancer (PCa). On the other hand, obesity has been linked to environmental influences, namely, the endocrine-disrupting chemicals capable of promoting adipogenesis and fat accumulation (obesogens). However, it is unknown whether obesogens can induce PPAT dysfunction, disrupting its crosstalk with PCa cells. The present study hypothesises that obesogens can target the PPAT, affecting its secretory activity and contributing to the development or aggressiveness of PCa. Through in vivo, ex vivo approaches and conditioned medium (CM) assays, we demonstrated that exposure to tributyltin (TBT), the first described obesogen, induced a PPAT "obese" phenotype, with adipocyte enlargement and enhanced secretion of leptin and C-C motif chemokine ligand 7 (CCL7). TBT-PPAT altered prostate cell fate, enhancing their viability, proliferation and migration, and reducing apoptotic rate. Moreover, it was shown that the TBT-PPAT secretome promoted the migration of prostate cells involving the C-C motif chemokine receptor 3 (CCR3). Overall, this study demonstrated the biological significance of TBT exposure, bringing functional evidence on the contribution of PPAT obesogenic dysregulation to prostate carcinogenesis. Moreover, it highlights the differences that may exist in PCa monitoring and treatment in obese vs. lean patients, pointing out the modulation of PPAT activity as a therapeutic target.

PMID:42217872 | DOI:10.1016/j.jes.2025.06.015

Environmentally relevant concentrations of tris(2-chloroethyl) phosphate disrupt zebrafish hypothalamus-pituitary-gonad-liver axis and transgenerational reproduction - May 30, 2026

J Environ Sci (China). 2026 Jul;165:715-723. doi: 10.1016/j.jes.2025.08.015. Epub 2025 Aug 12.

ABSTRACT

Tris(2-chloroethyl) phosphate (TCEP) is a widely used chlorinated organophosphorus flame retardant, that has been frequently detected in aquatic organisms and surface water. While previous studies have shown the potential endocrine disrupting effects of TCEP, its long-term reproductive toxicities at environmentally relevant concentrations remain unclear. This study comprehensively analyzed the reproductive toxicity and mechanisms of TCEP in zebrafish. Zebrafish were exposed to TCEP (0.2-200 µg/L) from embryo to adult stages for 120 days. Results showed significant alterations in reproductive indicators, including decreased body length and weight, reduced tissue indices and impaired gonadal development. Notably, TCEP altered sex hormone levels, with decreased 17β-estradiol (E2) and vitellogenin (VTG) in females, increased E2 and VTG in males, and reduced testosterone in both sexes. A female-biased sex ratio was observed at 22.01 and 241.84 µg/L TCEP, with reduced spawning and impaired F1 offspring development. Transcriptomic analysis revealed significant alterations in hypothalamus-pituitary-gonad-liver (HPGL) axis gene expression, such as hsd17b12a. Molecular docking simulations suggested that TCEP may interfere with sex hormone receptor binding and cytochrome P450 (CYP450) enzyme function. This study reveals new insights into the reproductive toxicity mechanisms of TCEP in zebrafish. The toxic effects follow an inverted U-shaped curve, with peak toxicity occurring at approximately 2.62 µg/L. These findings underscore the importance of regulating this emerging contaminant in freshwater ecosystems.

PMID:42217922 | DOI:10.1016/j.jes.2025.08.015

Dual-mode MXene-based biosensor coupled with machine learning: a smart sensing strategy for detection of zearalenone in food - May 30, 2026

Anal Chim Acta. 2026 Aug 15;1411:345620. doi: 10.1016/j.aca.2026.345620. Epub 2026 May 6.

ABSTRACT

BACKGROUND: Zearalenone (ZEN) is a potent endocrine disruptor that poses serious health risks through reproductive toxicity. Traditional detection methods, including high-performance liquid chromatography (HPLC), fall short in terms of speed, sensitivity, and portability for on-site food safety monitoring. This underscores the necessity of developing intelligent and field-deployable analytical strategies.

RESULTS: We reported a machine learning-enhanced sensing platform based on a dual-modal Ti₃C₂ MXene biosensor. The nanoprobe orchestrated fluorescence quenching and peroxidase-mimicking colorimetry in a single construct, converting ZEN concentration into two orthogonal optical readouts. The system achieved a detection limit of 0.35 ng mL^-1, improving to 0.27 ng mL^-1 upon algorithmic fusion. Validation of complex food matrices was conducted using spiked recovery experiments, with recovery rates ranging from 98.90% to 106.91% and a relative standard deviation consistently below 4.84%. Furthermore, in naturally contaminated samples, the results generated by this system were virtually identical to those obtained by high-performance liquid chromatography (HPLC), while significantly reducing analysis time, offering flexible mode selection, and providing cross-validation between the two orthogonal readouts.

SIGNIFICANCE AND NOVELTY: By unifying dual-modal transduction with machine-learning-driven data integration, this platform delivered sensitivity and accuracy surpassing conventional approaches while retaining field-deployable simplicity. It provided a robust solution for ZEN detection in real-world food samples, addressing a critical gap in rapid, on-site mycotoxin monitoring and advancing intelligent biosensing paradigms.

PMID:42217998 | DOI:10.1016/j.aca.2026.345620

A Systematic Review on Classification, Exposure Pathways of Micropollutants in the Aquatic Environment, and Its Associated Human Health Risks - May 30, 2026

J Appl Toxicol. 2026 May 29. doi: 10.1002/jat.70246. Online ahead of print.

ABSTRACT

Micropollutants are a diverse group of trace-level emerging contaminants present in different parts of the environment and causing notable risks to human health and aquatic life. They mainly originate from industrial, agricultural, pharmaceutical, and domestic sources, contaminating water bodies, where they induce toxicity in aquatic biota, bioaccumulate through food webs, and ultimately reach humans via ingestion, inhalation, and dermal exposure. Accumulating scientific research shows that exposure to micropollutants is associated with endocrine disruption, reproductive disorders, hormone-sensitive cancers, and dysfunction of the cardiovascular, respiratory, and immune systems. Their persistence, tendency to bioaccumulate, and chemically diverse modes of action further complicate their toxicological profiles. This systematic review evaluates findings from epidemiological, experimental, and molecular research published between 2000 and 2025 to provide a comprehensive perspective on micropollutant toxicity. Notably, it highlights critical research gaps, including inconsistent datasets, variation in defining chronic exposure, and limited investigation of combined or antagonistic effects of micropollutant mixtures. Addressing these gaps requires coordinated policy strategies, advances in remediation technology, and continuous scientific innovation to ensure public health protection and preserve the integrity of aquatic ecosystems. To bridge this gap, the present review proposes a systematic classification framework based on key sources, chemical nature, pathways, and ecotoxicological effects, while simultaneously elucidating their environmental dissemination in aquatic systems and characterizing their toxicological implications for both aquatic ecosystems and human health.

PMID:42216418 | DOI:10.1002/jat.70246

Environmental occurrence, exposure, toxicity, and transformation of benzothiazoles: A review - May 29, 2026

Eco Environ Health. 2026 Apr 24;5(2):100243. doi: 10.1016/j.eehl.2026.100243. eCollection 2026 Jun.

ABSTRACT

Benzothiazoles (BTs) are a class of aromatic heterocyclic compounds consisting of a benzene ring fused with a 1,3-thiazole ring. They have been widely used as vulcanization accelerators, fungicides, corrosion inhibitors, herbicides, anti-cancer drugs, etc., leading to their ubiquitous presence in various environmental media. Numerous studies have demonstrated that BTs exhibit multiple toxic effects. In this review, we systematically summarized research findings on the environmental occurrence, exposure, toxicity, and transformation of BTs. Benzothiazole (BTH) and 2-hydroxy-benzothiazole (2-OH-BTH) are the predominant BTs, with the highest detection frequencies and concentrations in environmental media and human biological samples. In some special cases, inhalation is estimated to be the primary exposure pathway, compared with ingestion and dermal contact. BTs have been reported to possess multiple toxic effects, including neurotoxicity, developmental and reproductive toxicity, endocrine-disrupting effects, and immunotoxicity. By integrating network toxicology analysis and reported experimental results, we highlighted that the aryl hydrocarbon receptor could be the key toxic target of BTs. BTs can further transform into diverse derivatives in wastewater treatment systems and the natural environment, with BTH and 2-OH-BTH being the main transformation products. The TP-Transformer model predicted that some BT-derived pharmaceuticals can be transformed into 2-amino-benzothiazole (2-ABTH), indicating that they are potential sources of environmental pollution. The predicted toxicity of most transformation products was reduced, while chlorinated derivatives exhibited increased toxic potential. Finally, we proposed BT-derived pharmaceuticals as a potential neglected source of BTs, and more attention should be given to the precise identification of transformation products and understanding the toxic mechanisms.

PMID:42211786 | PMC:PMC13213317 | DOI:10.1016/j.eehl.2026.100243

Breast cancer-related endocrine therapy on ocular surface microbiota: mechanism and clinical significance - May 29, 2026

Int J Ophthalmol. 2026 Jun 18;19(6):1194-1200. doi: 10.18240/ijo.2026.06.21. eCollection 2026.

ABSTRACT

Breast cancer is the leading malignancy among women worldwide, with endocrine therapy (e.g., selective estrogen receptor modulators, aromatase inhibitors) serving as a cornerstone of treatment; although these therapies are effective against hormone-sensitive breast cancer, they alter patients' systemic hormone profiles, which may disrupt the balance of the ocular surface microbiota that maintains ocular homeostasis. This review systematically examines the mechanisms of mainstream breast cancer endocrine therapies, the dynamics of the ocular surface microbiota, the association between hormonal imbalance and ocular surface homeostasis, as well as the relationship between ocular surface flora alterations, and therapy-related ocular complications, integrating evidence from oncology, endocrinology, and ophthalmology to propose research frameworks and prevention strategies for therapy-related ocular complications.

PMID:42211223 | PMC:PMC13213210 | DOI:10.18240/ijo.2026.06.21

Sleep Disorders in Klinefelter Syndrome and Other Sex Chromosome Aneuploidies: A Narrative Review - May 29, 2026

Andrology. 2026 May 29. doi: 10.1111/andr.70265. Online ahead of print.

ABSTRACT

BACKGROUND: Sex chromosome aneuploidies (SCAs) are among the most frequent types of chromosomal aneuploidies and include Klinefelter syndrome (47,XXY and higher-grade variants), 47,XYY syndrome, Turner syndrome (45,X), and trisomy X (47,XXX). These conditions share complex neurodevelopmental, endocrine, and metabolic features with important implications for reproductive and general health. Sleep plays a pivotal role in neurocognitive functioning, mood regulation, cardiometabolic homeostasis, and hypothalamic-pituitary-gonadal axis activity, yet sleep disorders remain poorly characterized and under-recognized in SCAs.

METHODS: This narrative review synthesizes current evidence on sleep disturbances in SCAs, with particular emphasis on male phenotypes, while integrating evidence from female SCAs to highlight shared mechanisms and overlapping sleep phenotypes.

RESULTS: Available data indicate an increased prevalence of insomnia, sleep fragmentation, excessive daytime sleepiness, circadian rhythm disturbances, and sleep-disordered breathing from childhood through adulthood. In Klinefelter syndrome, sleep alterations appear multifactorial, arising from the interaction between hypogonadism, obesity, psychiatric vulnerability, neurocognitive deficits, and possible circadian and melatonin dysregulation. Evidence in 47,XYY and higher-grade male SCAs, although limited, suggests a predominant contribution of neurodevelopmental and behavioral factors. Emerging findings also implicate oxidative stress as a potential mechanistic link between sleep disruption, metabolic dysregulation, and neurocognitive impairment.

CONCLUSIONS: Overall, the literature is fragmented and methodologically heterogeneous, underscoring the need for systematic sleep screening and integrated multidisciplinary management within andrological care pathways to improve long-term health and reproductive outcomes in individuals with SCAs.

PMID:42212520 | DOI:10.1111/andr.70265

Trans sodium crocetinate protects against hepatotoxicity induced by bisphenol A in rats - May 29, 2026

Iran J Basic Med Sci. 2026;29(4):570-577.

ABSTRACT

OBJECTIVES: Bisphenol A (BPA) is a monomer used in producing a wide range of materials and products, and it is recognized as an endocrine disruptor. Exposure to BPA can cause toxicity in multiple organs, especially the liver. Trans sodium crocetinate (TSC) is a synthetic salt derived from crocetin extracted from Crocus sativus. TSC exhibits antioxidant, anti-apoptotic, and properties that inhibit autophagy. This study evaluates the effects of TSC on liver toxicity induced by BPA.

MATERIALS AND METHODS: A total of 42 rats were allocated into seven groups, including those exposed to BPA at a dose of 75 mg/kg, BPA and trans sodium crocetinate (TSC) at doses of 10, 20, and 40 mg/kg, and groups receiving olive oil, distilled water, or TSC (40 mg/kg) alone. The total antioxidant capacity (TAC), lipid peroxidation, and glutathione, as well as serum aspartate aminotransferase (AST), alanine aminotransferase (ALT), lactate dehydrogenase (LDH), alkaline phosphatase (ALP), and total bilirubin were assessed using colorimetric methods. Reactive oxygen species (ROS) and liver protein expression were quantified using fluorimetric and western blot techniques.

RESULTS: TSC, at the dose of 40 mg/kg, reduced the levels of ROS and lipid peroxidation induced by BPA, while remarkably increasing the glutathione content and total antioxidant capacity (TAC) in liver tissue. Moreover, TSC markedly alleviated the BPA-induced increases in caspase-3 protein levels and in the activities of ALT, AST, ALP, and LDH, as well as in serum bilirubin T.

CONCLUSION: Altogether, TSC can be regarded as a supplement to protect against BPA-induced hepatotoxicity due to its potent antioxidant and anti-apoptotic effects.

PMID:42212217 | PMC:PMC13213438

Deoxynivalenol Impairs Ovarian Function by Triggering Ferroptosis in Granulosa Cells through GPX2 Inhibition and Oxidative Stress - May 29, 2026

J Agric Food Chem. 2026 May 29. doi: 10.1021/acs.jafc.6c02013. Online ahead of print.

ABSTRACT

Deoxynivalenol (DON), a mycotoxin produced by Fusarium species, is a widespread cereal contaminant that impairs swine growth and reproduction. Although DON-induced ovarian dysfunction has been reported, its underlying molecular mechanisms remain incompletely defined. We constructed DON exposure models in piglets and porcine ovarian granulosa cells to investigate conserved pathogenic mechanisms. Integrative transcriptomic and Cleavage Under Targets and Tagmentation (CUT&Tag) analyses identified GPX2 as a key target. DON inhibited glycolytic lactate production, reducing H3K18 lactylation at the GPX2 promoter and repressing transcription. GPX2 depletion disrupted redox homeostasis, induced oxidative stress and mitochondrial dysfunction, and triggered ferroptosis, impairing steroidogenesis. Ferrostatin-1 or GPX2 overexpression alleviated DON-induced injury and restored endocrine function. These pathogenic effects were conserved in DON-treated mice, confirming evolutionary conservation across mammals. Collectively, our findings reveal a metabolically and epigenetically regulated GPX2-glutathione-ferroptosis axis mediating DON ovarian toxicity, providing a potential therapeutic target for mitigating mycotoxin-related reproductive disorders.

PMID:42210900 | DOI:10.1021/acs.jafc.6c02013

Weight-of-evidence assessment of the endocrine-disrupting properties of propylene oxide - May 29, 2026

Crit Rev Toxicol. 2026 May 29:1-25. doi: 10.1080/10408444.2026.2649597. Online ahead of print.

ABSTRACT

Propylene oxide (PO) is a high-production-volume chemical widely used as an industrial intermediate and classified as carcinogen and mutagen in humans. Despite its regulatory significance, a comprehensive evaluation of its endocrine-disrupting (ED) potential has not been previously conducted. This review applies a weight-of-evidence (WoE) approach, integrating data from regulatory dossiers, peer-reviewed literature, publicly accessible databases, and in silico predictions to assess whether PO meets internationally accepted ED criteria. Available evidence indicates that PO does not exhibit endocrine activity via estrogenic, androgenic, steroidogenic, thyroid (EATS), or non-EATS pathways, as supported by negative quantitative structure-activity relationship (QSAR) predictions and absence of mechanistic effects in vivo. Similarly, adverse outcomes observed in repeated-dose, reproductive, and developmental toxicity studies were either secondary to systemic toxicity, inconsistent, or unrelated to endocrine modes of action. Epidemiological findings suggesting associations with breast cancer, diabetes, or obesity were limited by methodological uncertainties and lack of causal inference. Collectively, the WoE demonstrates that PO should not be classified as an endocrine-disrupting chemical for humans or wildlife, although data gaps remain for environmental receptors and metabolites.

PMID:42213097 | DOI:10.1080/10408444.2026.2649597

Early-onset colorectal cancer in Australia: environmental, microbial, and policy implications - May 29, 2026

Dig Dis. 2026 May 29:1-10. doi: 10.1159/000552644. Online ahead of print.

ABSTRACT

BACKGROUND: Early-onset colorectal cancer (EOCRC; age <50 years) is rising in Australia despite improving outcomes in older adults. EOCRC shows a strong birth-cohort effect, disproportionate growth in left-sided and rectal tumours, and more frequent stage III-IV presentation. Most cases occur without a family history, indicating that environmental and biological pressures are accelerating carcinogenesis in otherwise average-risk hosts.

OBJECTIVE: To summarise current evidence on EOCRC aetiology, emphasising microbial, dietary and chemical exposures, and to outline clinical, policy and research priorities for Australia.

DISCUSSION: Traditional risks such as obesity, metabolic syndrome, sedentary behaviour, alcohol and smoking likely contribute via insulin resistance, chronic inflammation and IGF-1-mediated signalling, but they do not fully explain the recent acceleration or distal predominance. Hereditary syndromes account for a minority of EOCRC, and tumour driver mutation patterns broadly resemble later-onset colorectal cancer, supporting earlier triggering rather than novel genetics. Convergent evidence implicates gut dysbiosis and exposures that disrupt mucosal defences or cause direct DNA damage. Colibactin-producing Escherichia coli can induce a distinctive mutational signature that appears enriched in early and distal tumours. Microplastics and plasticisers may impair barrier function and promote low-grade inflammation, while PFAS and related endocrine-disrupting chemicals are linked to metabolic and immune perturbation and altered bile acid biology. Cumulative antibiotic exposure, particularly early in life, may reduce microbial diversity and favour pathobionts such as Fusobacterium nucleatum.

PMID:42213629 | DOI:10.1159/000552644

Early-onset colorectal cancer in Australia: environmental, microbial, and policy implications - May 29, 2026

Dig Dis. 2026 May 29:1-10. doi: 10.1159/000552644. Online ahead of print.

ABSTRACT

OBJECTIVE: To summarise current evidence on EOCRC aetiology, emphasising microbial, dietary and chemical exposures, and to outline clinical, policy and research priorities for Australia.

PMID:42213629 | DOI:10.1159/000552644

Immunomodulatory effects of Bisphenol A, perfluorooctanoic acid, and tris(1,3-dichloro-2-propyl) phosphate on THP-1-derived macrophages - May 29, 2026

Environ Int. 2026 May 21;213:110321. doi: 10.1016/j.envint.2026.110321. Online ahead of print.

ABSTRACT

Endocrine-disrupting chemicals (EDCs) are widespread environmental contaminants known to interfere with hormonal and immune functions. Among these, Bisphenol A (BPA), tris(1,3-dichloro-2-propyl) phosphate (TDCPP), and perfluorooctanoic acid (PFOA) are of significant concern due to their widespread human exposure and differing physicochemical profiles. Given that macrophages can represent early immune targets following EDC exposure, this study investigated the immunomodulatory effects of these structurally diverse compounds on THP-1-derived macrophage-like model. Cell viability was evaluated following 24 h exposure to a range of concentrations (1-100 µM), from which three doses (10, 50, 100 µM) were selected for functional assays. A follow-up viability assay at 48 h was performed to confirm the cellular impact of prolonged exposure. BPA and PFOA showed limited effects on cell viability, whereas TDCPP produced the most pronounced reduction. To assess immunomodulation, NFκB phosphorylation and cytokine production were evaluated under basal and LPS-stimulated conditions. BPA showed minimal effects across endpoints. TDCPP elicited modest NFκB activation, and under LPS stimulation, selectively attenuated specific cytokine responses. PFOA induced robust NFκB activation without corresponding changes in the measured cytokines, suggesting dissociation between upstream NFκB signaling and cytokine output in this model. Overall, these findings indicate compound-specific effects of BPA, TDCPP and PFOA in THP-1-derived macrophage-like cells and support the utility to this in vitro platform for comparative immunotoxicity screening and hypothesis generation. Future work integrating such data with quantitative in vitro-to-in vivo extrapolation (QIVIVIE/IVIVE) and more complex immune models may further improve human relevance.

PMID:42214231 | DOI:10.1016/j.envint.2026.110321

Effects of phthalate metabolite mixture exposure on mouse oocyte development - May 29, 2026

Environ Int. 2026 May 27;213:110332. doi: 10.1016/j.envint.2026.110332. Online ahead of print.

ABSTRACT

Phthalates are pervasive endocrine-disrupting chemicals widely used in consumer products. The wide use of many phthalates results in chronic human exposure to complex mixtures rather than single compounds. Despite extensive studies on individual compounds, the combined effects of phthalate metabolites on oogenesis remain poorly understood. Here, we developed a precise microinjection-based single-oocyte toxicological assay to examine the impact of a defined phthalate metabolite mixture on meiotic progression. Phthalate mixture exposure markedly impaired oocyte maturation, as most oocytes failed to extrude the first polar body. Mechanistic analyses revealed severe meiotic defects, including disrupted spindle morphology, chromosome misalignment, disorganized actin cytoskeleton, and impaired mitochondrial function, accompanied by excessive reactive oxygen species (ROS) accumulation and DNA damage. Single-cell transcriptomic profiling further identified differentially expressed genes enriched in biological processes related to exocytosis, secretory pathway regulation, and cytoskeletal organization, as well as in MAPK, JAK-STAT, cGMP-PKG, and GnRH signaling pathways that are essential for follicular development and oocyte maturation. Together, these findings demonstrate that combined phthalate exposure directly compromises female gamete quality and underscore the importance of evaluating mixture effects when assessing risks to women's reproductive health.

PMID:42214232 | DOI:10.1016/j.envint.2026.110332

The RFX6 mechanism spine: A unified model linking transcriptional coordination to endocrine resilience and diabetes pathogenesis - May 29, 2026

Life Sci. 2026 May 28:124501. doi: 10.1016/j.lfs.2026.124501. Online ahead of print.

ABSTRACT

Glucose homeostasis requires coordinated insulin, glucagon, and incretin secretion across pancreatic and gastrointestinal endocrine systems. Despite heterogeneous genetic and environmental triggers, diabetes converges on β-cell dysfunction and disrupted inter-endocrine coordination. Regulatory Factor X6 (RFX6) is essential for endocrine development and remains expressed in adult islets and enteroendocrine cells; however, its functions have largely been studied in isolated contexts. Here, we integrate developmental, epigenomic, physiological, and genetic evidence into a hypothesis-generating framework in which RFX6 functions as a dosage-sensitive endocrine regulator. RFX6-associated programs are linked to glucose sensing, membrane excitability, insulin secretion, redox stability, and gut-islet signaling. Available genetic and functional evidence supports a model in which graded reduction in RFX6 activity correlates with a spectrum of phenotypes: biallelic loss causes syndromic neonatal diabetes (Mitchell-Riley syndrome), heterozygous variants are linked to impaired insulin secretion in RFX6-MODY, and common regulatory variants near the RFX6 locus contribute to polygenic type 2 diabetes. We propose a five-tier "Mechanism Spine" linking chromatin regulation to endocrine physiology and clinical phenotype while emphasizing that translational implications remain preliminary.

PMID:42214606 | DOI:10.1016/j.lfs.2026.124501

miR-to-miR interactions: investigating the effects of miR-21 down-regulation and bisphenol exposure in COCs, arrested 8-cell embryos and blastocysts - May 29, 2026

Reprod Toxicol. 2026 May 28:109270. doi: 10.1016/j.reprotox.2026.109270. Online ahead of print.

ABSTRACT

Endocrine disrupting compounds (EDCs) including bisphenol A (BPA), bisphenol S (BPS) and bisphenol F (BPF) have the potential to alter microRNAs (miRs) expression and elicit negative effects on reproduction. miR-21 is one of the most dynamic miRs, abundantly expressed in oocytes and embryos, and is affected by BPA exposure. miR-21 dysregulation and bisphenol exposure might influence key miRs (miR-10b, -29a, -34c, -103a, -130, -146, -155, -224, -378, and -499) important for oocyte maturation, embryonic genome activation (EGA) and early embryonic development. We aimed to test the hypothesis that expression of key miRs during oocyte maturation and in vitro embryo production is affected by anti-miR-21 and bisphenols in a miR-21-dependent manner, shedding light on the concept of miR-to-miR interaction. miR-21 may positively co-regulate apoptotic pathways with miR-103a, miR-155 and miR-29a, and inversely with miR-34c, and participate in a shared pathway for progesterone signalling with miR-155. These processes may have implications in regulating each other's biogenesis or feedback loops. Proper oocyte maturation is vital for oocyte competence and resulting embryo development; thus, reduced maturation rates (p<1×10^-11) resulted in lower cleavage (p=0.001) and blastocyst rates (p=0.0022) in anti-miR-21 and BPA, BPS, and BPF groups. Additionally, apoptosis, detected in blastocysts using TUNEL staining, showed that BPA, BPS and BPF treatment increased DNA fragmentation (p<0.05). Overall, this study deepens our understanding of miR-to-miR interactions and the effect of EDCs on epigenetic modulation affecting oocyte competence and in vitro early embryonic development, ultimately aimed at improving Artificial Reproductive Technologies in humans and animals.

PMID:42214639 | DOI:10.1016/j.reprotox.2026.109270

PAX4 R192H variant impairs beta cell function by disrupting beta cell identity and compensatory capacity in response to metabolic stress - May 29, 2026

Genome Med. 2026 May 28. doi: 10.1186/s13073-026-01669-z. Online ahead of print.

ABSTRACT

BACKGROUND: Type 2 diabetes is characterized by progressive β cell dysfunction, yet the mechanisms by which genetic susceptibility contributes to β cell area and function remain poorly understood. PAX4 is a transcription factor critical for β cell development, and a nonsynonymous variant resulting in an arginine-to-histidine substitution at position 192 (R192H) has been associated with increased type 2 diabetes risk and identified only in individuals of East Asian ancestry.

METHODS: Here, we generated PAX4 R192H knock-in (Pax4^R192H/R192H) mouse and integrated metabolic phenotyping, bulk and single cell transcriptomics, and human cohort analyses to investigate how PAX4 R192H mutation increases the risk of type 2 diabetes.

RESULTS: Homozygote knock-in mice (Pax4 R192H) exhibited normal pancreatic endocrine development but developed glucose intolerance and impaired insulin secretion when fed a high-fat diet. Bulk and single-cell RNA-seq of islets from Pax4 R192H mice fed high-fat diet revealed impaired β cell adaptation to metabolic stress characterized by enhanced endoplasmic reticulum stress and impaired β cell maturity, with upregulation of dedifferentiation and α cell markers and downregulation of β cell identity genes. Pax4 deletion in β cells resulted in similar phenotypic and transcriptomic profiles to Pax4 R192H mice. In humans, the trajectories of β cell function were evaluated over a 14-year period using biennial oral glucose tolerance tests from 4,242 participants, where PAX4 R192H carriers showed 1.4-fold accelerated decline in disposition index, with increasing body mass index further exacerbating their type 2 diabetes risk.

CONCLUSIONS: Overall, PAX4 is essential for maintaining β cell identity and compensatory function under metabolic stress, and the R192H variant predisposes to type 2 diabetes by impairing this adaptive capacity.

PMID:42210309 | DOI:10.1186/s13073-026-01669-z

Regimen-dependent glucocorticoid effects improve muscle performance without altering CNS physiology in mdx mice - May 29, 2026

J Physiol. 2026 May 28. doi: 10.1113/JP291378. Online ahead of print.

ABSTRACT

Duchenne muscular dystrophy (DMD) is a multisystem disorder affecting striated muscle, metabolism and the central nervous system (CNS). Although glucocorticoids remain the standard therapy, muscle-centric evaluations typically fail to capture how dosing regimen and compound selection affect CNS and metabolic phenotypes. Here, we compared daily and weekly dosing of prednisolone and vamorolone in juvenile mdx mice over 6 weeks to determine how these variables influence multisystem outcomes. Multiorgan efficacy and adverse effects were quantified across behavioural, endocrine, metabolic, cardiovascular and muscle domains using behavioural assays, in vivo and functional muscle testing, haemodynamic evaluation and histopathology. Daily glucocorticoid dosing failed to improve muscle function or strength, whereas weekly vamorolone produced the most robust improvements in functional and in vivo muscle strength. Daily prednisolone reduced circulating creatine kinase levels, but this biochemical change did not translate into enhanced muscle function outcomes. Daily regimens also induced severe adrenal cortical atrophy, yet these endocrine alterations were dissociated from CNS stress and anxiety responses, which remained unchanged by treatment. In addition, daily dosing caused pronounced systemic metabolic consequences, whereas weekly regimens substantially attenuated these effects, identifying dosing frequency as a key determinant of safety. Together, these findings demonstrate that glucocorticoid regimen selection fundamentally reshapes the efficacy versus adverse effect profile and underscores the value of integrated multiorgan evaluation in DMD. This work highlights the need to expand therapeutic assessments beyond muscle pathology and raises new questions about how glucocorticoid signalling differentially engages peripheral and central physiological systems. KEY POINTS: Duchenne muscular dystrophy affects multiple physiological systems, yet current glucocorticoid assessments rarely capture the CNS and metabolic effects of dosing regimens. Weekly vamorolone dosing improved muscle strength in mdx mice, while daily prednisolone failed to improve performance despite lowering plasma creatine kinase. Stress- and anxiety-related behaviours remained unchanged, despite adrenal atrophy revealing a disconnect between peripheral endocrine disruption and CNS phenotypes. Daily glucocorticoid regimens triggered endocrine and metabolic side effects, whereas weekly dosing reduced these effects. Prednisolone and vamorolone produced broadly similar systemic side-effect profiles, but dosing frequency was the primary determinant of their severity.

PMID:42210563 | DOI:10.1113/JP291378

Mitochondrial myopathy biomarkers - May 29, 2026

Adv Clin Chem. 2026;133:161-216. doi: 10.1016/bs.acc.2026.01.007. Epub 2026 Feb 20.

ABSTRACT

Mitochondrial myopathies comprise a heterogeneous group of disorders arising from structural or functional mitochondrial impairments that disrupt oxidative phosphorylation and cellular ATP production. The resulting energy deficit manifests not only in muscle but frequently leads to multi-systemic disease involving the brain, heart, kidneys, and endocrine system, creating a complex and often confounding clinical presentation. A critical, often overlooked aspect of their pathophysiology is that mitochondrial dysfunction extends far beyond bioenergetics. These organelles are vital hubs for biosynthetic pathways, calcium homeostasis, thermogenesis, apoptosis, and redox-sensitive signaling pathways that govern gene expression. The disruption of these integrated functions, whose molecular consequences are still being elucidated, is central to the disease's progression and heterogeneity. This clinical and molecular complexity contributes to significant diagnostic delay, with many remaining undiagnosed. Therefore, the development and strategic implementation of reliable biomarkers are essential. This review critically evaluates current and emerging biomarkers, proposing a diagnostic framework designed to improve diagnostic accuracy, limit unnecessary procedures, and ensure timely access to therapeutic interventions and genetic counseling.

PMID:42215146 | DOI:10.1016/bs.acc.2026.01.007

Early-onset colorectal cancer in Australia: environmental, microbial, and policy implications - May 29, 2026

Dig Dis. 2026 May 29:1-10. doi: 10.1159/000552644. Online ahead of print.

ABSTRACT

OBJECTIVE: To summarise current evidence on EOCRC aetiology, emphasising microbial, dietary and chemical exposures, and to outline clinical, policy and research priorities for Australia.

PMID:42213629 | DOI:10.1159/000552644

Breast Cancer Risk and Screening in Active Duty Military Members and Veterans - May 28, 2026

J Breast Imaging. 2026 May 28:wbag004. doi: 10.1093/jbi/wbag004. Online ahead of print.

ABSTRACT

Women represent a growing demographic within the United States military, both active duty and veterans. Breast cancer is the most prevalent non-dermatologic malignancy among female active duty members and veterans. Military service members, specifically women aged 40-59 years, have a higher incidence of breast cancer compared to the general population. Retrospective cohort studies of military members suggest that work-related reproductive factors, including higher frequency of contraceptive use and shorter duration of breastfeeding, may account for at least part of the higher incidence. The impact, if any, of military environmental exposures, such as volatile organic compounds, endocrine disrupting chemicals, pesticides, airborne hazards, and open burn pits, on breast cancer risk is an area of ongoing investigation. This article aims to advance understanding of breast cancer, risk, treatment, and outcomes in military populations while examining current screening practices and ongoing efforts to strengthen prevention and early detection among active duty service members and veterans. The potential of the SERVICE Act to increase screening access in certain military members under age 40 years will be emphasized. Efforts to improve breast cancer prevention and early detection for active duty service members and veterans are imperative for preserving military force readiness and essential for the health of the all-volunteer force of the United States military.

PMID:42207118 | DOI:10.1093/jbi/wbag004

Multi-target protective effects of Pterostilbene against BPA-induced reproductive toxicity revealed by integrative network pharmacology and in vivo validation - May 28, 2026

Tissue Cell. 2026 May 25;102:103639. doi: 10.1016/j.tice.2026.103639. Online ahead of print.

ABSTRACT

Pterostilbene (PT) is a naturally occurring dimethylated analogue of resveratrol with improved lipophilicity and metabolic stability, yet its role in male reproductive toxicity remains largely unexplored. Using an adult male zebrafish model, this study investigated the protective effects of PT against bisphenol A (BPA)-induced reproductive dysfunction. Adult male zebrafish were randomly assigned to five groups: control, BPA, BPA + PT-L (5 mg/kg), BPA + PT-H (10 mg/kg), and BPA + icariin (ICA, 10 mg/kg). Exposure to BPA (3000 μg/L) resulted in pronounced testicular damage, disrupted spermatogenesis, decreased testosterone levels, and elevated oxidative stress. Administration of PT (5 or 10 mg/kg) markedly improved gonadal morphology and function, restored gonadosomatic index and testosterone levels, and enhanced sperm quality and DNA integrity. Additionally, PT treatment attenuated oxidative damage by reducing reactive oxygen species and lipid peroxidation and by re-establishing endogenous antioxidant capacity. Integrated analyses combining network pharmacology, molecular docking, and gene expression validation indicated that PT acts through multiple targets and pathways associated with cell survival, oxidative stress regulation, and endocrine signaling, including PI3K/Akt, mTOR, MAPK/FoxO, and estrogen-related pathways. These findings suggest that PT may mitigate BPA-induced male reproductive toxicity through coordinated redox and endocrine regulatory mechanisms.

PMID:42208228 | DOI:10.1016/j.tice.2026.103639

Efficacy of an e-Learning Module on Endocrine Disruptors for Family Medicine Residents: Matched Before-And-After Cohort Study - May 28, 2026

JMIR Form Res. 2026 May 28;10:e89880. doi: 10.2196/89880.

ABSTRACT

BACKGROUND: Environmental factors account for 23% of global deaths and 25% of chronic diseases. In France, the Fourth National Environmental Health Plan prioritizes training health professionals in environmental health. Endocrine-disrupting chemicals (EDCs) are chemical substances that interfere with hormonal systems, contributing to a range of health effects. In 2024, the Primary Care and Environmental Health (PCEH) program at the University of Montpellier-Nîmes introduced an innovative e-learning module on EDCs for first-year family medicine residents.

OBJECTIVE: This study aimed to evaluate the impact of the PCEH e-learning module on participants' satisfaction, knowledge, and self-reported behaviors regarding EDCs in household environments.

METHODS: This monocentric, matched before-and-after cohort study included all first-year family medicine residents at the University of Montpellier-Nîmes. The module, developed collaboratively by clinicians and educators, integrated interactive images, artificial intelligence-generated virtual rooms, short educational videos, games, and flash cards. Participants were assessed using pretraining and posttraining questionnaires administered immediately before and after the module. These questionnaires evaluated satisfaction (using a 5-point Likert scale), knowledge (using binary "yes" or "no" questions), and behaviors (using a 5-point Likert scale). Statistical analyses included the McNemar test for paired categorical variables and paired 2-tailed t tests for continuous variables, with a significance threshold set at a P value of less than .05.

RESULTS: This study aimed to evaluate the impact of an e-learning module on knowledge and behaviors related to endocrine disruptors. Our findings show significant improvements across all measured domains. Of 148 eligible residents, 78 (52.7%) completed both assessments over a 17-day period. Overall satisfaction was high (mean 4.0/5, SD 0.9), with positive ratings for the e-learning format (mean 4.1/5, SD 1.0) and module duration (mean 4.2/5, SD 1.0). Knowledge improved significantly, with a mean 55.56 (SD 13.54) increase in correct identification of EDCs across all substances (P<.001). Self-reported behaviors improved by an average of 2.13 points (95% CI 1.71-2.56) on the 5-point scale (P<.001), exceeding those reported in previous PCEH modules. Secondary outcomes showed high posttraining identification of at-risk populations and exposure locations, although recognition of some substances (eg, alkylphenols and phenoxyethanol) remained low.

CONCLUSIONS: This innovative e-learning module significantly improved residents' knowledge and preventive behaviors related to EDCs. These findings support the integration of environmental health training into medical curricula and highlight the potential of scalable e-learning interventions to strengthen preventive competencies in primary care.

PMID:42207575 | DOI:10.2196/89880

Hesperidin Mitigates Bisphenol-A Induced Oxidative Stress, Endocrine Disruption and Testicular Damage in Adult Male Wistar Rats - May 28, 2026

J Exp Pharmacol. 2026 May 22;18:595476. doi: 10.2147/JEP.S595476. eCollection 2026.

ABSTRACT

INTRODUCTION: Bisphenol A (BPA), a well-known endocrine disruptor, is newly emerging as causing male infertility by endocrine disturbances, induction of oxidative stress and testicular toxicity. This study investigates the protective role of hesperidin against BPA-induced testicular toxicity in male Wistar rats.

METHODOLOGY: The rats were divided into six groups (n=7): control (normal saline); BPA-only (50 mg/kg); hesperidin-only at 50 mg/kg and 100 mg/kg; and two pre-treated groups receiving hesperidin (50 and 100 mg/kg) followed by BPA (50 mg/kg). All treatments were administered orally for 8 weeks. Post-treatment analyses included testicular weight, volume, and diameter measurements; serum testosterone, FSH, and LH levels; oxidative stress markers (MDA, SOD, CAT, GPx, and GSH); and histological and morphometric evaluation of the testis.

RESULT AND DISCUSSION: BPA exposure significantly reduced testicular dimensions, decreased serum testosterone, FSH, and LH. Histopathological examination revealed degeneration of seminiferous tubules, germ-cell depletion, reduced counts of spermatogonia, spermatocytes, spermatids, Sertoli and Leydig cells. BPA significantly induced oxidative stress, evidenced by increased MDA and decreased SOD, CAT, GPx, and GSH. Hesperidin significantly mitigated these effects by restoring testicular morphology, hormonal profiles, enhancing oxidative stress markers, improving histology and cell populations.

CONCLUSION: Hesperidin demonstrates protective properties against BPA-induced testicular and endocrine toxicity in rats, likely as a result of its antioxidant properties.

PMID:42205862 | PMC:PMC13207936 | DOI:10.2147/JEP.S595476

Pro-aging effects of chronic glucocorticoid signaling - May 28, 2026

Cell Metab. 2026 May 28:S1550-4131(26)00187-7. doi: 10.1016/j.cmet.2026.05.002. Online ahead of print.

ABSTRACT

Glucocorticoids (GCs) are essential endocrine regulators coordinating stress responsiveness, metabolic flexibility, inflammatory resolution, and circadian physiology. While acute GC fluctuations are adaptive, sustained exposure (arising from psychosocial stress, circadian disruption, obesity, chronic inflammation, neoplasms, or steroid therapy) elicits pleiotropic effects that overlap with biological aging. Prolonged GC signaling intersects with multiple hallmarks of aging by altering nutrient sensing, suppressing autophagy, impairing mitochondrial quality control, and promoting cellular senescence. In this context, the GC-responsive polypeptide ACBP/DBI (acyl-coenzyme A [CoA]-binding protein/diazepam-binding inhibitor) has emerged as a stress-induced inhibitor of macroautophagy that amplifies several metabolic and immune consequences of GC excess linked to aging phenotypes. Clinically, chronic GC elevation is associated with earlier and more severe manifestations of age-related diseases, including metabolic syndrome, osteoporosis, sarcopenia, neurodegeneration, cardiovascular disease, immunosenescence, and cancer. Here, we review mechanistic links between GC signaling and systemic aging and discuss strategies to mitigate the age-accelerating consequences of persistent GC exposure.

PMID:42208534 | DOI:10.1016/j.cmet.2026.05.002

Hereditary PCOS and the environmental toxicant F-53B converge on lipid metabolic reprogramming to impair fetal brain development - May 28, 2026

Ecotoxicol Environ Saf. 2026 May 28;319:120302. doi: 10.1016/j.ecoenv.2026.120302. Online ahead of print.

ABSTRACT

Polycystic ovary syndrome (PCOS) is associated with an increased risk of neurodevelopmental disorders in offspring, yet how maternal PCOS interacts with environmental toxicants to influence fetal brain development remains unclear.We hypothesized that an AMH-programmed PCOS-like background increases neurodevelopmental vulnerability, which is worsened by gestational F-53B exposure through lipid metabolic reprogramming. Our study reveals how endocrine-metabolic dysfunction and environmental toxicants interact to impact fetal brain development. F0 dams were exposed to anti Müllerian hormone in late gestation to generate PCOS like F1 females and simultaneously received F-53B or vehicle, yielding four groups: Con, AMH, F-53B, and AF. F1 females from AMH lineages exhibited reproductive abnormalities characteristic of PCOS, which were most pronounced in the AF group. Bulk RNA sequencing of E14.5 F2 embryonic brains revealed progressive transcriptomic divergence across groups, with AF embryos showing the greatest shift from controls. Genes differentially expressed in both the F-53B vs Con and AF vs AMH comparisons were enriched in lipid metabolism and PPAR-related pathways, accompanied by graded upregulation of Cidec, Plin1, Fabp4, and Pparg and reciprocal downregulation of Aqp7, which was confirmed at the protein level for CIDEC, PLIN1, and AQP7. At the cellular level, AF embryos exhibited the most severe neurodevelopmental defects, including loss of TBR2⁺ positive intermediate progenitors, reduced TBR1⁺ and SATB2⁺ cortical neurons, diminished Neurod1⁺ and Tuj1⁺ expression, and decreased Olig2⁺ positive oligodendroglial cells. We hypothesized that an AMH-programmed PCOS-like background would prime offspring for subtle neurodevelopmental vulnerability, F-53B exposure during pregnancy would induce lipid metabolic reprogramming in the offspring fetal brain, and the combination of AMH-induced PCOS-like programming and F-53B exposure would exert 'two-hit' effects, leading to the greatest disruption of neurogenesis and gliogenesis. By linking an emerging PFAS alternative to mechanistically grounded alterations in fetal brain lipid metabolism and neural lineage development on a PCOS-like background, our work provides an integrated framework for understanding how endocrine-metabolic disorders and environmental contaminants converge to shape neurodevelopmental risk.

PMID:42208382 | DOI:10.1016/j.ecoenv.2026.120302

Screening 16 bisphenol analogues in asthenospermia: BPM-CDK1 axis identified by computational and In Vitro validation - May 28, 2026

Reprod Toxicol. 2026 May 27;143:109268. doi: 10.1016/j.reprotox.2026.109268. Online ahead of print.

ABSTRACT

Bisphenol A (BPA) is a ubiquitous industrial chemical found in numerous consumer products. While its endocrine-disrupting effects and reproductive toxicity are well-documented, the widespread use of structural analogues (BPs) as "BPA-free" alternatives has raised urgent concerns regarding their comparable health risks. In this study, we employed a systematic network toxicology framework to evaluate the pathogenic mechanisms of 16 bisphenol congeners in asthenospermia. Through an integrated screening of disease-target associations, five lead compounds-BPA, BPS, BPB, BPP, and BPM-were identified as having the most significant correlation with sperm motility disorders. To elucidate the underlying molecular mechanism, core targets were identified via Protein-Protein Interaction (PPI) networks and further prioritized using LASSO regression, Random Forest (RF), Logistic Regression (LR), Naive Bayes (NB), Support Vector Machine (SVM), and Extreme Gradient Boosting (XGBoost). Molecular docking analysis revealed that CDK1 exhibited the most robust binding affinity to these BPs (lowest docking energy of -10.4 kcal/mol), a finding further validated by molecular dynamics simulations showing high structural stability of the BPM-CDK1 complexes. Notably, among the prioritized congeners, BPM emerged as a critical modulator of this signaling node. In vitro experiments demonstrated that BPM exposure significantly impaired the migration of GC-2spd(ts) and TM4 cells. Furthermore, BPM treatment markedly downregulated CDK1 expression at both the mRNA and protein levels. These results suggest that BPs contribute to the pathogenesis of asthenospermia by disrupting cell proliferation and cycle regulation, specifically through the BPM-mediated suppression of the CDK1 axis.

PMID:42208629 | DOI:10.1016/j.reprotox.2026.109268

Molecular mechanisms underlying metamifop-induced chronic toxicity in Daphnia magna: Insights from metabolic detoxification, oxidative stress, and endocrine disruption - May 28, 2026

Comp Biochem Physiol C Toxicol Pharmacol. 2026 May 27:110584. doi: 10.1016/j.cbpc.2026.110584. Online ahead of print.

ABSTRACT

Metamifop (MET) is frequently detected in aquatic environments and threatens non-target aquatic organisms, yet chronic toxicological data on aquatic invertebrates remain scarce. To evaluate the physiological and molecular mechanisms of MET toxicity, Daphnia magna was subjected to 21-day chronic exposure at 0, 0.4, 4, and 40 μg/L. Results showed a pronounced concentration-dependent growth and reproductive toxicity, evidenced by a reduced the offspring number at the first brood in the 0.4 μg/L treatment, while 4 and 40 μg/L MET further decreased the total number of offspring per female and the body length of D. magna. MET impaired digestive function by altering the mRNA expression levels of α-amylase, trypsin, and α-esterase, disrupted energy metabolism by downregulating ak expression, lowering ATP content, and decreasing ATPase activity, and inhibited metabolic detoxification mechanisms via reduced transcriptional levels of cyp360a8, gst, and p-gp genes. Exposure to 40 μg/L MET also significantly decreased the swimming speed of D. magna. MET further induced oxidative stress in D. magna, as supported by diminished SOD and CAT activity, downregulated transcription of trx and trxr, decreased levels of hsp70 and hsp90, and elevated contents of GSH and MDA. Reduced expression of the nvd, ecr, cyp314, and vtg genes indicated impairment of ecdysteroid signaling system. Collectively, these findings demonstrate that prolonged MET exposure exerts adverse effects on growth and reproduction that are closely associated with disturbed energy metabolism, detoxifying capacity, antioxidant defense, and ecdysteroid signaling system in D. magna, highlighting the ecological hazards of MET to aquatic ecosystems.

PMID:42208721 | DOI:10.1016/j.cbpc.2026.110584

Iodoacetic acid causes developmental toxicity in zebrafish - May 28, 2026

Toxicol Sci. 2026 May 28:kfag062. doi: 10.1093/toxsci/kfag062. Online ahead of print.

ABSTRACT

Water disinfection can generate disinfection byproducts (DBPs) such as iodoacetic acid (IAA) by reacting with organic matter in water supplies. In vitro studies have shown that IAA is a cytotoxic and genotoxic DBP. In vivo studies using animal models further indicate that IAA has toxic effects on reproductive function and the endocrine system. Yet, its developmental toxicity remains unknown. In this study, we show that exposure to IAA at concentrations ranging from 1 to 100 µM induces dose-dependent embryonic mortality, with the greatest sensitivity observed during the first 24 hours of development. Sublethal concentrations cause delayed or failed hatching and disrupt the development of multiple vital organs. Notably, IAA exposure impairs swim bladder inflation, reduces otolith size, and decreases heart rate. Moreover, IAA reduces intestinal mucus production by suppressing genes essential for mucin production. Given the crucial role of intestinal mucus in defending against pathogens and maintaining host and gut microbiota homeostasis, the deleterious effect of IAA on mucus production highlights its potential pathogenic role in driving disorders linked to epithelial barrier dysfunction and microbiome dysfunction. Together, these findings demonstrate that IAA induces pronounced developmental toxicity affecting multiple organ systems in zebrafish. This study provides the first in vivo evidence that IAA disrupts embryonic development and intestinal function.

PMID:42210016 | DOI:10.1093/toxsci/kfag062

Zearalenone exposure and the mammalian gut microbiome: A systematic review of the literature - May 28, 2026

Toxicol Sci. 2026 May 28:kfag064. doi: 10.1093/toxsci/kfag064. Online ahead of print.

ABSTRACT

Mycotoxins are fungal derived metabolites found in the global food supply, particularly in cereal grains and processed foods. Zearalenone (ZEN), one of the more common mycotoxins, widely contaminates human food supplies at concentrations above established maximum contamination levels. However, the effects of ZEN exposure on human health have only begun to be explored, with most studies on this topic focusing on its endocrine-disrupting effects in the reproductive system. ZEN is readily absorbed following oral administration, making the gastrointestinal (GI) tract and its microbiota primary targets for toxicity. The gut microbiome plays a critical role in nutrient processing and immune function and can be heavily influenced by dietary and chemical exposures. Given widespread human dietary exposure to ZEN, we conducted a comprehensive literature review of ZEN and its metabolites in relation to the mammalian gut microbiome. We identified 19 studies, all conducted in animal models, and each reported alterations in gut microbiome composition in ZEN-treated groups compared to control animals. Several papers reported modified metabolism in ZEN-treated groups, particularly related to short chain fatty acids. In light of this small but compelling literature and the expected increase in mycotoxin contamination due to the industrialization of the food supply and warmer weather conditions, we identified several priority areas for future study. These include better understanding the mechanisms by which ZEN and its metabolites affect the microbiome and ultimate translation to human health.

PMID:42210027 | DOI:10.1093/toxsci/kfag064

Hereditary PCOS and the environmental toxicant F-53B converge on lipid metabolic reprogramming to impair fetal brain development - May 28, 2026

Ecotoxicol Environ Saf. 2026 May 28;319:120302. doi: 10.1016/j.ecoenv.2026.120302. Online ahead of print.

ABSTRACT

PMID:42208382 | DOI:10.1016/j.ecoenv.2026.120302

Iodoacetic acid causes developmental toxicity in zebrafish - May 28, 2026

Abstract

Zearalenone exposure and the mammalian gut microbiome: A systematic review of the literature - May 28, 2026

Abstract

In-Utero Exposure to Electronic Waste Heavy Metals and Adverse Pregnancy and Neonatal Outcomes: A Systematic Review - May 27, 2026

Int J Environ Res Public Health. 2026 May 18;23(5):665. doi: 10.3390/ijerph23050665.

ABSTRACT

Electronic waste (e-waste) recycling releases heavy metals into surrounding environments, creating potential health risks for nearby populations, particularly pregnant women and developing fetuses. This systematic review evaluated human evidence linking prenatal exposure to heavy metals originating from informal e-waste recycling with adverse pregnancy and neonatal outcomes. Electronic databases, including PubMed and Scopus, were searched through 23 September 2025, for studies measuring heavy metal exposure among pregnant women or neonates living in e-waste-affected communities. Following the Navigation Guide methodology, eight observational studies met the inclusion criteria and were assessed for risk of bias and strength of evidence. Across studies, concentrations of heavy metals were higher in exposed populations and were detected in maternal blood, placenta, cord blood, urine, and meconium samples from exposed populations. Prenatal exposure was consistently associated with adverse outcomes, with many studies reporting statistically significant associations between heavy metal exposure and reduced birth weight, length, head circumference, gestational age, neonatal body mass index, lower Apgar scores, impaired neonatal neurobehavioral development, placental molecular alterations, endocrine disruption, and increased neonatal DNA damage. Overall, the evidence was rated as moderate quality with sufficient evidence linking prenatal heavy-metal exposure from e-waste to impaired fetal growth and neonatal development, and limited evidence for pregnancy complications. These findings highlight the need for improved regulation of e-waste recycling and strengthened public health protections for vulnerable populations.

PMID:42196757 | PMC:PMC13206999 | DOI:10.3390/ijerph23050665

Sex-Specific sRNA Signatures in Rat Liver Reveal Divergent Alterations Following Perinatal Exposure to Glyphosate and Its Mixture with 2,4-D and Dicamba - May 27, 2026

Int J Mol Sci. 2026 May 9;27(10):4221. doi: 10.3390/ijms27104221.

ABSTRACT

Perinatal exposure to environmental toxicants, even at regulatory relevant doses, can disrupt molecular programming during critical developmental windows, with long-term consequences for organ function and disease risk. We investigated sex-specific hepatic microRNA (miRNA) responses in Wistar rats following perinatal exposure to glyphosate at European Union (EU) acceptable daily intake (ADI) dose (0.5 mg/kg bw/day), at no-observed-adverse-effect level (NOAEL; 50 mg/kg bw/day), and mixed with 2,4-D (0.3 mg/kg bw/day) and dicamba (0.02 mg/kg bw/day), each at their ADI. Using small RNA sequencing, we identified distinct miRNA expression profiles in males and females, with the mixture inducing the most pronounced divergence (52 differentially expressed miRNAs between males and females). Functional enrichment analysis of validated miRNA targets revealed activation of apoptotic, oncogenic, and stress-related pathways in males, alongside downregulation of homeostatic and anti-fibrotic regulators. Females showed suppression of miRNAs involved in hormone signaling, development, and tissue regeneration, suggesting endocrine and adaptive disruption. Our findings highlight the importance of determining effects based on sex and sensitive developmental stages in toxicological assessment, since different regulatory programs may be involved in the response of males and females to xenobiotics. The identified miRNAs may represent early biomarkers of hepatic dysfunction following early-life herbicide exposure, supporting their utility in future risk evaluations.

PMID:42196204 | PMC:PMC13207187 | DOI:10.3390/ijms27104221

The Impact of Endocrine Disruptor Exposure During Pregnancy on Bacterial Complications and Viral Infections: A Narrative Review - May 27, 2026

Microorganisms. 2026 Apr 30;14(5):1012. doi: 10.3390/microorganisms14051012.

ABSTRACT

Endocrine-disrupting chemicals (EDCs) are a diverse group of environmental pollutants capable of interfering with hormonal and immune system regulation. In recent years, increasing concern has been raised about the effects of chemicals, including bisphenols, phthalates, per- and polyfluoroalkyl substances (PFAS), insecticides, and parabens, on maternal and fetal health, primarily due to their widespread exposure in human populations. Pregnancy represents a critical window characterized by tightly regulated hormonal and immunological adaptations. Emerging evidence suggests that EDC exposure during this period may alter maternal microbiota, disrupt immune responses, and interfere with endocrine signaling. These changes may increase susceptibility to bacterial and viral infections, including bacterial vaginosis, urinary tract infections, and intrauterine infections, all of which are associated with adverse pregnancy outcomes. This review summarizes the current evidence on the sources and mechanisms of exposure to endocrine disruptors during pregnancy and examines the potential biological pathways linking endocrine disruption to the development of infections. Particular emphasis is placed on the interactions between immune regulation, hormonal signaling, and changes in the microbiome, which may contribute to increased susceptibility to infections. A deeper understanding of these complex mechanisms is critical to improve risk assessment, develop effective public health strategies, and ultimately protect maternal and fetal health in an environment of increasing chemical exposure. A literature search was conducted using PubMed/MEDLINE, Scopus, and Web of Science, including studies published up to January 2026.

PMID:42197398 | PMC:PMC13209177 | DOI:10.3390/microorganisms14051012

Toxicological Assessment of 17β-Estradiol and 17α-Ethinylestradiol After Adsorption in a Biomass Filter Associated with the Nanomaterial δ-FeOOH - May 27, 2026

Int J Environ Res Public Health. 2026 May 20;23(5):677. doi: 10.3390/ijerph23050677.

ABSTRACT

Emerging contaminants pose significant risks to ecosystems yet are not routinely included in standard monitoring or regulatory frameworks. Among these substances, endocrine disruptors such as β-estradiol and 17α-ethinylestradiol threaten both human and environmental health by interfering with metabolism, reproduction, and development across multiple species. These hormones are continuously released into the environment through excretion and improper disposal, and conventional water treatment processes are largely ineffective at removing them. As a result, they can accumulate in aquatic organisms and enter the human food chain. Recent studies have demonstrated that banana peel, Pleurotus ostreatus biomasses, and the nanomaterial δ-FeOOH are efficient, low-cost materials for the removal of toxic metals, suggesting their potential applicability for eliminating estrogenic compounds. Therefore, this study aimed to evaluate the removal of β-estradiol and 17α-ethinylestradiol using filters composed of banana peel and P. ostreatus biomass combined with δ-FeOOH. Hormone removal efficiency was assessed by LC-MS, and toxicity reduction was evaluated through bioassays. The results showed up to 100% removal of hormone concentrations and a significant decrease in sample toxicity, indicating that this filtration system represents a safe and effective alternative for removing organic contaminants from water.

PMID:42196769 | PMC:PMC13206398 | DOI:10.3390/ijerph23050677

Green Coffee Extract Mitigates Fipronil-Induced Endocrine Disruption, Metabolic Disturbances and Oxidative Stress in Male Albino Rats - May 27, 2026

Toxics. 2026 Apr 30;14(5):383. doi: 10.3390/toxics14050383.

ABSTRACT

This study evaluated the protective effects of green coffee (Coffea arabica L.) extract (GCE) against metabolic and endocrine disturbances induced by fipronil (FIP) in male rats. Animals were randomly allocated into four groups (n = 6): control, GCE (100 mg/kg), FIP (4.85 mg/kg), and combined FIP + GCE, and treated orally for 90 days. FIP exposure significantly impaired glucose homeostasis, as indicated by a 14.8% increase in the oral glucose tolerance test (OGTT) response and a 2.4-fold increase in the homeostatic model assessment of insulin resistance (HOMA-IR). It also disrupted lipid metabolism, with marked elevations in triglycerides (74.10%) and total cholesterol (57.55%). Endocrine imbalance was evident, including increased resistin levels (113.86%) and reduced triiodothyronine (T3; -37.5%), adiponectin (-42.73%), and high-density lipoprotein (HDL; -9.31%). Oxidative stress and inflammation were significantly enhanced, as demonstrated by elevated malondialdehyde (MDA; +93.56%) and pro-inflammatory cytokines (IL-1β: +246.56%; IL-6: +275%), alongside a reduction in total antioxidant capacity (TAC; -45.24%). Additionally, serum albumin levels decreased markedly (-54%). Co-administration of GCE significantly improved metabolic, hormonal, and inflammatory parameters, including insulin resistance (HOMA-IR). Histopathological analysis further confirmed its protective effects on hepatic and renal tissues. Overall, GCE mitigates FIP-induced metabolic and endocrine dysfunction, likely through its antioxidant and anti-inflammatory properties.

PMID:42198509 | PMC:PMC13211167 | DOI:10.3390/toxics14050383

Toxicological Effects and Health Impacts of Per- and Polyfluoroalkyl Substances (PFAS) in Humans - May 27, 2026

Toxics. 2026 Apr 26;14(5):374. doi: 10.3390/toxics14050374.

ABSTRACT

Per- and polyfluoroalkyl substances (PFAS) are a class of synthetic chemicals notable for their high persistence and extensive applications. With the advancement of detection technologies in recent years, PFAS have been frequently identified in environmental media and human biological samples, raising significant global concerns about their potential health risks. PFAS exhibit distinctive toxicokinetic behaviors, including efficient absorption, strong protein binding, limited metabolism, and slow excretion, which lead to prolonged biological half-lives and considerable bioaccumulation in humans. These properties contribute to a range of adverse health outcomes, such as endocrine disruption, immune suppression, liver damage, reproductive toxicity, carcinogenic potential, and cardiovascular disease. This review synthesizes evidence on PFAS-associated health risks from a multisystem, multitarget perspective, elucidating the key molecular pathways involved, thereby providing a scientific basis for understanding their complex toxicological effects and for developing targeted prevention and control strategies. Future research should prioritize characterizing the toxicological profiles of individual PFAS compounds, evaluating the health impacts of combined (mixture) exposures, and assessing risks associated with chronic, low-dose exposure to support the development of public health strategies and regulatory decisions.

PMID:42198500 | PMC:PMC13211586 | DOI:10.3390/toxics14050374

The central role of hyperandrogenism in driving metabolic dysfunction in polycystic ovary syndrome: from pathophysiological mechanisms to targeted therapies - May 27, 2026

J Ovarian Res. 2026 May 26. doi: 10.1186/s13048-026-02124-8. Online ahead of print.

ABSTRACT

Polycystic ovary syndrome is a prevalent endocrine disorder wherein hyperandrogenism plays a central pathogenic role that extends beyond its reproductive manifestations. This review systematically elucidates the pathophysiological mechanisms through which hyperandrogenism, acting in a vicious cycle with insulin resistance, drives systemic metabolic dysfunction. We synthesize evidence demonstrating that hyperandrogenism promotes organ-specific lipotoxicity and insulin resistance. This contributes to visceral adiposity, hepatic steatosis (and its progression to metabolic dysfunction-associated steatotic liver disease), and skeletal muscle dysfunction. Furthermore, we explore the detrimental effects of hyperandrogenism on cardiovascular integrity and gut microbial homeostasis. Based on this mechanistic framework, we evaluate current therapeutic strategies, drawing a key distinction between metabolic-focused interventions (e.g., lifestyle modifications, insulin-sensitizing agents) that disrupt the hyperandrogenism-insulin resistance cycle, and androgen-lowering therapies (e.g., combined oral contraceptives) that primarily alleviate symptoms with limited metabolic benefits. We conclude that redefining hyperandrogenism as a primary metabolic driver is crucial for developing targeted strategies that mitigate the long-term metabolic risks associated with polycystic ovary syndrome.

PMID:42192468 | DOI:10.1186/s13048-026-02124-8

Occurrence, Distribution, and Risk Assessment of Phenolic Endocrine-Disrupting Chemicals in Surface Waters of the World's Longest Water Diversion Project: The Non-Negligible Impact of Local Wastewater Emissions - May 27, 2026

Toxics. 2026 May 13;14(5):427. doi: 10.3390/toxics14050427.

ABSTRACT

Water contamination by phenolic endocrine-disrupting chemicals (EDCs) is a global environmental concern. Yet, the occurrence of phenolic EDCs in artificial water diversion systems remains poorly understood. Thus, the Eastern Route of the South-to-North Water Diversion Project, the world's longest water diversion project, was chosen as the study area to investigate the spatiotemporal distribution of alkylphenols (APs) and bisphenol A (BPA), typical phenolic EDCs, and to evaluate their risks. During the diversion operation, higher mean ΣAP concentrations were observed in lakes of Nansi and Dongping relative to the Luoma Lake-Dongping Lake and Yangtze-Luoma Lake diversion channels. The AP composition in the two lakes was also different from that in the two channels. These findings demonstrated that the canal water was not a key source of AP contamination in the lakes, highlighting the importance of local wastewater inputs. The spatial distribution of ΣAP and BPA concentrations in the lakes was mainly affected by the riverine inputs. For ecological risks, 4-n-nonylphenol (4-n-NP) exhibited moderate ecological risks at 81.3% of sampling sites in Dongping Lake and 68.8% of those in Luoma Lake, highlighting the need for heightened attention in future studies. Even under the high exposure scenario, 4-n-NP and BPA would not produce health risks to residents through water intakes. Overall, surface water resources of the Eastern Route Project were confirmed to be safe for human consumption.

PMID:42198553 | PMC:PMC13211472 | DOI:10.3390/toxics14050427

Biological responses to heat stress in livestock: From thermoregulation to cellular and epigenetic adaptation - May 27, 2026

J Therm Biol. 2026 May 1;139:104473. doi: 10.1016/j.jtherbio.2026.104473. Online ahead of print.

ABSTRACT

Climate change driven increases in ambient temperature have positioned heat stress (HS) as a major biological constraint on livestock productivity and welfare. Excessive thermal load disrupts thermoregulatory balance, reduces feed intake and digestive efficiency, and perturbs immune and endocrine function, culminating in impaired energy metabolism and systemic dysfunction. Reproductive processes show pronounced thermal sensitivity, as HS alters hypothalamic-pituitary-gonadal axis signaling, compromises gametogenesis, reduces embryo viability, and suppresses fertility. Productive traits, including milk yield, growth rate, egg production, and carcass quality, decline as cumulative heat load exceeds adaptive capacity. Emerging evidence identifies the gut-brain axis as a critical mediator of HS pathology, where heat-induced vascular redistribution, epithelial hypoxia, and microbiome dysbiosis amplify inflammatory and metabolic stress. At the cellular level, HS triggers mitochondrial dysfunction, oxidative imbalance, activation of heat shock responses, immune dysregulation, and epigenetic remodeling with potential long-term consequences. Current mitigation strategies encompass nutritional and phytogenic modulation of stress pathways, genetic selection for thermo-tolerance, microclimate control, and precision livestock farming (PLF) technologies for real-time detection of thermal strain. However, partial understanding of molecular thresholds, epigenetic plasticity, and integrative system responses limits effective translation. Addressing these gaps through mechanistically driven and interdisciplinary research is essential for enhancing thermal resilience and sustaining livestock production under ongoing climate warming.

PMID:42202371 | DOI:10.1016/j.jtherbio.2026.104473

A network toxicology and molecular docking study predicting putative molecular targets and pathways linking bisphenol a exposure to diffuse large B-cell lymphoma - May 27, 2026

Discov Oncol. 2026 May 27. doi: 10.1007/s12672-026-05274-9. Online ahead of print.

ABSTRACT

Bisphenol A (BPA) is a pervasive environmental endocrine disruptor implicated in hormone-related cancers.However, its association with non-hormone-dependent malignancies such as Diffuse Large B-cell Lymphoma (DLBCL) remains poorly understood.This study aimed to predict the potential molecular mechanisms linking BPA exposure to DLBCL pathogenesis through an integrated approach combining network toxicology and molecular docking.We systematically identified 46 overlapping genes shared between BPA-associated targets and DLBCL-related genes. Protein-protein interaction network analysis indicate six hub genes(HSP90AB1, HSPA8, CCNA2, CDK1, LDHA, and HSPA14),with HSP90AB1 exhibiting the highest topological centrality.Functional enrichment analysis demonstrated that these genes are significantly enriched in key oncogenic signaling pathways, including the PI3K-Akt and MAPK pathways, as well as critical biological processes such as protein folding and cell cycle regulation. Molecular docking simulations further predicted the stable binding affinity between BPA and each of the six hub proteins, with binding energies below - 6.0 kcal/mol. Collectively, our computational findings suggest a putative mechanistic framework in which BPA may contribute to DLBCL development by directly interacting with and potentially dysregulating central regulatory nodes in cellular networks, particularly the molecular chaperone HSP90AB1. These predictions require experimental validation but provide a basis for future mechanistic studies.

PMID:42201521 | DOI:10.1007/s12672-026-05274-9

Chronic exposure to sodium fluoride or to tebuconazole disrupts the thyroid hormone and immune systems during early development of rainbow trout (Oncorhynchus mykiss) - May 27, 2026

Aquat Toxicol. 2026 May 19;297:107867. doi: 10.1016/j.aquatox.2026.107867. Online ahead of print.

ABSTRACT

Over the past 20 years, there has been a growing interest in endocrine-disrupting chemicals (EDCs) found in both terrestrial and aquatic environments. These substances have garnered attention from scientists, the public and regulatory bodies, with many being classified as substances of very high health concern. Only recently, disruption of the thyroid hormone system (THS) by EDCs has also attracted significant attention: In vertebrates, the THS interacts with various physiological systems, including the immune system (IS), and plays a crucial role in development. It can also influence the microbial diversity in certain tissues. The main objective of this study was to investigate the potential impact of sodium fluoride (NaF) on the THS and IS in rainbow trout (Oncorhynchus mykiss), a species of both economic and environmental importance. For this end, trout were exposed from the embryonic stage (48 h post-fertilisation) to the juvenile stage for 7 months. Fish were subjected to 1.5 mg F^-/L or 5 mg F^-/L and 20 µg/L tebuconazole (TBZ; positive control) monitored daily and sampled after 3 and 7 months of exposure to assess potential disruption to the thyroid hormone and immune systems. Results document that chronic exposure to NaF or TBZ during early life stages of rainbow trout induces a broad range of sublethal effects, including physiological condition, immune competence, endocrine regulation and organ morphology. Although mortality was reduced, most probably due to the antifungal activity of TBZ, the consistent alterations observed in thyroid hormone dynamics and immune parameters clearly indicate a deterioration of overall health.

PMID:42202487 | DOI:10.1016/j.aquatox.2026.107867

Tailored covalent organic frameworks with tunable fluorine groups for efficient adsorption of bisphenol analogues - May 27, 2026

J Hazard Mater. 2026 May 19;513:142433. doi: 10.1016/j.jhazmat.2026.142433. Online ahead of print.

ABSTRACT

Bisphenol analogues (BPs) are widespread endocrine-disrupting contaminants that threaten ecosystems and human health. Herein, covalent organic frameworks (COFs) with tunable fluorine groups were designed to achieve efficient adsorption of BPs. By systematically regulating the number of fluorine groups in the monomers, it was demonstrated that the adsorption of BPs did not increase monotonically with fluorination; instead, an optimal structure-function balance was achieved at moderate fluorine substitution. The optimized fluorinated COF exhibited high adsorption capacities of 779.60, 416.69, and 559.74 mg/g for bisphenol A (BPA), bisphenol F (BPF), and bisphenol S (BPS), respectively, representing increases of 79.43%, 55.03%, and 148.46% compared with the non-fluorinated COF. To improve recyclability and practical applicability, the optimized COF was integrated with chitosan (CS) to construct monolithic COF/CS aerogels. The aerogels showed further capacity enhancements of 24.27-30.66% and significantly accelerated adsorption kinetics, with pseudo-second-order rate constants increasing by ≥ 168.18%. Mechanistic studies revealed that the adsorption of BPs was governed by pore filling, π-π stacking, hydrogen bonds, and hydrophobic interactions. The aerogels were successfully applied in food pretreatment and environmental water treatment, demonstrating efficient enrichment, strong anti-interference capability, and good reusability.

PMID:42202520 | DOI:10.1016/j.jhazmat.2026.142433

Microplastics as both a driver of genitourinary cancers and a deliverer of treatments - May 27, 2026

Commun Med (Lond). 2026 May 27;6(1):311. doi: 10.1038/s43856-026-01675-7.

ABSTRACT

Microplastics and nanoplastics (MNPs) are environmental contaminants increasingly detected in human tissues, raising public health concerns. Although evidence is still insufficient to directly link MNPs to genitourinary cancers (GU), this Review examines their potential role in prostate, bladder, and renal cell carcinoma. Proposed mechanisms include chronic inflammation, oxidative stress, genotoxicity, and endocrine disruption driven by plastic-associated additives. Emerging studies report quantitative detection of MNPs within human prostate and bladder tumors, with higher burdens associated with dietary habits such as frequent take-out food consumption. The Review also highlights their role in cancer therapy: MNPs may alter antineoplastic drug pharmacokinetics and promote resistance, yet polymer-based nanoparticles can be engineered as advanced drug delivery platforms. Materials such as PLGA and PEG may improve targeted delivery of chemotherapies and immunotherapies, supporting more effective and personalized treatment strategies in GU oncology.

PMID:42203887 | PMC:PMC13216587 | DOI:10.1038/s43856-026-01675-7

Comparing the Effects of Glyphosate and Mycotoxins in the Human Follicular Microenvironment: An Exploratory Exposome Study - May 27, 2026

Biomedicines. 2026 May 9;14(5):1081. doi: 10.3390/biomedicines14051081.

ABSTRACT

Background: Exposure to anthropogenic and/or natural (e.g., herbicides or mycotoxins) endocrine-disrupting chemicals (EDCs) has been linked to several reproductive disorders. Glyphosate (GLY), a common agricultural agent, is a potential element of the exposome that bioaccumulates and has potential endocrine and oxidative stress-related effects. However, data on its presence in the human ovarian microenvironment remain limited. Our study examined GLY levels in follicular fluid (ff) and serum and their relationships with oxidative stress markers, reproductive hormones, and stress hormones in women undergoing in vitro fertilization (IVF). Methods: 50 women undergoing controlled ovarian stimulation participated. Serum and ff samples were routinely collected during oocyte retrieval. GLY, related hormones (e.g., cortisol, estradiol-E2, anti-Müllerian hormone-AMH, and melatonin-MT), an oxidative stress marker malondialdehyde (MDA), antioxidant enzyme activities, total antioxidant capacity, and co-occurring natural pollutant mycotoxin levels were measured. Relationships between GLY levels and these mediators were assessed using correlation and regression analyses. Results: GLY was detected in both serum and ff at similar concentrations (0.038 ± 0.006 ng/mL vs. 0.045 ± 0.006 ng/mL; p = 0.414). Follicular GLY levels showed a positive association with MDA (Spearman's r = 0.4487, p < 0.001), explaining 28.6% of the variability in follicular MDA. Serum GLY was positively associated with serum (β = 40.26, p = 0.0058) and follicular E2 (r = 0.29, p = 0.042). Serum GLY levels were negatively correlated with cortisol (β = -0.0188, p = 0.020). A slight correlation between follicular GLY and MT was observed (p = 0.03). No associations were found between GLY levels and age, body mass index, AMH, the recombinant gonadotropin dose used, antioxidant enzyme activities, follicle count, oocyte yield, or embryo viability. Conclusions: This study might be the first to demonstrate the presence of GLY of exposome in human ff, indicating that environmental exposure to GLY may reach the oocyte microenvironment. The correlation with lipid peroxidation suggests GLY could contribute to follicular oxidative stress. The associations with E2 and cortisol point to potential endocrine-disrupting effects. While no direct impact on IVF outcomes was observed, findings suggest low-level exposure to GLY could influence ovarian physiology through specific biochemical mechanisms.

PMID:42193405 | PMC:PMC13204281 | DOI:10.3390/biomedicines14051081

Exposure to Endocrine Disruptors and Stress Hormones Across Pregnancy Trimesters: Links with Maternal Telomere Length - May 27, 2026

J Xenobiot. 2026 May 7;16(3):82. doi: 10.3390/jox16030082.

ABSTRACT

BACKGROUND: Exposure of pregnant women to stress and endocrine-disrupting chemicals (EDCs) during pregnancy can have a substantial impact on mother and infant health. We investigated the concentrations of EDCs, such as parabens (PBs) and triclosan (TCS), as well as stress hormones (cortisone and cortisol), across pregnancy trimesters and examined their associations with maternal average telomere length (TL).

METHODS: Hair samples from 49 postpartum women were analyzed using liquid chromatography-mass spectrometry (LC-MS) to quantify EDCs and stress hormone concentrations.

RESULTS: The mean methyl paraben concentrations in the hair of postpartum women were prevalent across all pregnancy trimesters, while butyl paraben was detected at the lowest levels. The mean concentration of PBs followed the order methyl > propyl > ethyl > benzyl > butyl paraben across pregnancy trimesters. We found that ethyl paraben and triclosan were each positively and significantly associated with cortisol levels in postpartum women's hair. Consistent with this, the mean cortisone concentration gradually increased from the first to the third pregnancy trimester, whereas cortisol reached the highest mean concentration at the second trimester. A significant positive association between cortisol and cortisone levels was observed. Further analyses revealed that mothers' average TL was positively associated with ethylparaben and triclosan levels and inversely associated with benzylparaben levels. Last but not least, we found that cortisol/cortisone levels were positively associated with postpartum women's TL in a statistically significant manner.

CONCLUSIONS: In the present study, prenatal exposure to stress hormones and EDCs appears to exert a statistically significant impact on maternal TL dynamics.

PMID:42201077 | PMC:PMC13214751 | DOI:10.3390/jox16030082

A cross-sectional study on the associations between serum metal exposure and thyroid hormones in chinese pregnant women - May 27, 2026

Sci Rep. 2026 May 27. doi: 10.1038/s41598-026-51478-y. Online ahead of print.

ABSTRACT

Prenatal exposure to environmental metals has been increasingly recognized as a crucial factor influencing maternal thyroid function, which plays a vital role in regulating metabolism, maintaining pregnancy, and supporting fetal neurodevelopment. However, the effects of emerging or less-studied metals, such as titanium (Ti), selenium (Se), and strontium (Sr), on thyroid hormone homeostasis during pregnancy remain poorly understood. In this cohort of 495 pregnant women, 12 of 19 metals showed detection frequencies above 90%. After adjusting for major confounders, Ti exposure was negatively associated with Total triiodothyronine (FT4), while Se and Sr showed consistent inverse associations with Total triiodothyronine (TT3) and Free triiodothyronine (FT3), indicating potential disruption of thyroid hormone synthesis and conversion. Mixture analyses using WQS and BKMR further identified key metals contributing to altered thyroid hormone levels and suggested heterogeneous directions of association within the metal mixture. These findings reveal previously unrecognized associations between Ti, Se, Sr, and maternal thyroid hormone alterations, providing new insights into the endocrine effects of environmental metal exposure. This study expands the understanding of how both essential and non-essential metals influence maternal thyroid function, emphasizing the need for stricter environmental monitoring and preventive strategies to protect maternal endocrine health and optimize fetal developmental outcomes.

PMID:42204214 | DOI:10.1038/s41598-026-51478-y

Toxicological Effects and Health Impacts of Per- and Polyfluoroalkyl Substances (PFAS) in Humans - May 27, 2026

Toxics. 2026 Apr 26;14(5):374. doi: 10.3390/toxics14050374.

ABSTRACT

PMID:42198500 | PMC:PMC13211586 | DOI:10.3390/toxics14050374

PFOA Damages Blood-Testis Barrier Integrity in Mice by Inhibited Glycolysis Caused H3K18 Lactylation Modification Impairment - May 27, 2026

Toxics. 2026 May 7;14(5):399. doi: 10.3390/toxics14050399.

ABSTRACT

The molecular mechanism underlying male reproductive toxicity associated with Perfluorooctanoic acid (PFOA), a persistent environmental endocrine disruptor (EDC), has not yet been fully elucidated. Six-week-old male C57BL/6 mice were treated with PFOA by oral gavage at 0, 1.25, 5, 10, and 20 mg/kg/day for 35 days to explore its toxic effects on the male reproductive system and the underlying mechanisms. Analyses of semen quality, testicular histopathology, and blood-testis barrier (BTB) integrity revealed that PFOA caused dose-dependent structural and functional damage to the BTB, leading to markedly reduced semen quality. Based on transcriptomic sequencing and differential gene enrichment analysis, the glycolytic pathway was identified as a key regulatory target for PFOA-induced damage to the reproductive system. Further validation revealed that PFOA exposure inhibited glycolysis-related enzymes (Hexokinase 1 (HK1), Glucose Transporter 1 (GLUT1), and Lactate Dehydrogenase A (LDHA)), reduced lactate production and ATP synthesis, lowered Pan-Kla and H3K18la levels, and diminished H3K18la enrichment at the Hk1, Glut1, and Ldha promoters, whereas exogenous sodium lactate reversed these changes. This study is the first to identify the "glycolysis-lactate-H3K18la" chain as a key regulator in PFOA-induced BTB damage and spermatogenesis impairment, offering a new theoretical foundation for understanding EDC-induced male reproductive toxicity.

PMID:42198526 | PMC:PMC13211035 | DOI:10.3390/toxics14050399

The Impact of Endocrine Disruptor Exposure During Pregnancy on Bacterial Complications and Viral Infections: A Narrative Review - May 27, 2026

Microorganisms. 2026 Apr 30;14(5):1012. doi: 10.3390/microorganisms14051012.

ABSTRACT

PMID:42197398 | PMC:PMC13209177 | DOI:10.3390/microorganisms14051012

Beyond Blast Injury: Occupational Hygiene, Safety, and Toxicology Considerations for Mixed-Metal and Energetic-Chemical Exposures to Explosive Ordnance Disposal Personnel - May 27, 2026

Toxics. 2026 Apr 28;14(5):379. doi: 10.3390/toxics14050379.

ABSTRACT

Explosive ordnance (EO), including AXO (abandoned explosive ordnance), IEDs (improvised explosives devices), and UXO (unexploded ordnance), are widely recognised for their blast and fragmentation hazards, but they also represent a persistent and under-addressed source of occupational chemical exposure for explosive ordnance disposal (EOD) personnel. EOD core activities liberate mixed metals and energetic chemicals, resulting in exposures that are multi-route (inhalation of dusts and fumes, dermal loading amplified by sweat and glove occlusion, and ingestion via hand-to-mouth transfer during eating, drinking, or smoking) and multi-temporal (repeated low-dose background plus task-driven spikes), as well as chemically complex. Clinically, this can present as syndromic overlap across acute and chronic domains, with symptoms that are easily misattributed to heat stress, dehydration, infection, or fatigue. Acute effects of concern include neurotoxic presentations (headache, dizziness, confusion, tremor, and seizure), respiratory and mucosal irritation following dust or fume events, gastrointestinal symptoms, and patterns suggestive of acute hepatic or renal stress, particularly when high-intensity tasks occur in hot environments that compound physiologic strain. Chronic outcomes relevant to repeatedly exposed EOD personnel include renal function decline, neurocognitive effects that can degrade operational decision making and safety, persistent haematologic abnormalities, and endocrine disruption signals, with long-latency risks requiring cautious interpretation given sparse longitudinal data and confounding co-exposures. This review synthesises the current evidence base through an EOD lens and translates it into pragmatic clinical and programmatic actions: task-based exposure characterisation; tiered biomonitoring and medical surveillance aligned to operational tempo; incident-triggered assessment pathways after high-residue events; and prevention strategies that work under field constraints, including contamination control zones, hygiene enforcement, glove and respiratory protection optimisation, tool and vehicle decontamination, and measures to prevent secondary transfer and take-home exposure. The central takeaway is practical: EOD programs can reduce morbidity and improve readiness by treating explosive ordnance as a chemical mixture exposure problem, adopting mixture-aware clinical triage, and embedding surveillance and controls that match how EOD work is actually performed.

PMID:42198505 | PMC:PMC13211267 | DOI:10.3390/toxics14050379

Emerging Environmental Contaminants Targeting Cardiovascular Ion Channels: Exposure Effects, Underlying Mechanisms, and Implications for Cardiovascular Health Risks - May 27, 2026

Toxics. 2026 May 21;14(5):450. doi: 10.3390/toxics14050450.

ABSTRACT

Emerging contaminants (ECs) encompass a wide spectrum of pollutants, from endocrine disruptors and persistent organic pollutants to microplastics and pharmaceutical residues. These contaminants often exhibit distinct chemical and physical properties compared with traditional pollutants and potentially pose risks to human health, especially as they have become pervasive in environmental and biological systems. ECs can also pose a significant threat to cardiovascular health, as they may target the ion channels that are critical to regulating cardiac excitability and contraction. However, the impact of ECs on the cardiovascular system, particularly on cardiac ion channels, remains elusive. In this review, we aim to provide an overview of the knowledge base concerning the impact of emerging contaminants on cardiac ion channels, with an emphasis on the effects of these compounds on cardiac excitability, contractility, and overall cardiovascular function. We first outline the structural and functional characteristics of ion channels, along with how these transmembrane proteins regulate cardiac physiology. Subsequently, we detail how typical ECs directly or indirectly interact with various ion channels-including sodium, calcium, potassium channels, as well as ion transporters and exchangers. Special attention is given to studies that have demonstrated cell-level responses or examined how pollutant concentration and chemical structure affect the modulation of ion channels. This review compiles recent research reports to elucidate the mechanisms by which EC exposure disrupts cardiac ion channels, potentially leading to cardiotoxicity. Moreover, the insights gathered herein illuminate critical research gaps and outline essential directions for future investigations.

PMID:42198576 | PMC:PMC13211365 | DOI:10.3390/toxics14050450

Optimized Zebrafish In Vitro Maturation with Real-Time Morphometric Workflow Reveals Inhibition by 1,2-Bis(2,4,6-tribromophenoxy)ethane (BTBPE) - May 27, 2026

Toxics. 2026 Apr 25;14(5):368. doi: 10.3390/toxics14050368.

ABSTRACT

Novel brominated flame retardants (NBFRs), including 1,2-bis(2,4,6-tribromophenoxy)ethane (BTBPE), are emerging endocrine-disrupting chemicals, though their direct effects on female gamete maturation remain insufficiently characterized. In this study, we used a refined zebrafish oocyte in vitro maturation (IVM) model integrating germinal vesicle breakdown (GVBD) assessment with real-time, image-based oocyte diameter quantification. The workflow incorporated donor-condition optimization and diameter-based quality control during sorting. Oocytes from donors 4 to 5 months post-fertilization (mpf) showed more consistent diameter dynamics at the dish level than those from donors 3 to 4 mpf. Mixed-sex co-housing was associated with higher GVBD and larger Δdiameter than separated housing, although this comparison should be considered preliminary. Under DHP induction, BTBPE (1-1000 nM) consistently suppressed GVBD and attenuated maturation-associated diameter increases, with a non-monotonic-like response pattern. These findings indicate that BTBPE impairs oocyte maturation competence in vitro and supports real-time morphometric tracking as a practical QC component for zebrafish IVM workflows.

PMID:42198495 | PMC:PMC13211186 | DOI:10.3390/toxics14050368

Epigenetic regulation of non-coding DNA in placental development and disorders - May 27, 2026

Epigenomics. 2026 May 27:1-14. doi: 10.1080/17501911.2026.2678924. Online ahead of print.

ABSTRACT

The human placenta is an epigenetically exceptional organ that must execute rapid proliferation, lineage bifurcation, and controlled invasion while maintaining immune tolerance at the maternal-fetal interface. Trophoblast lineages operate within a developmentally programmed "pseudo-malignant" regulatory state, characterized by global DNA hypomethylation, large partially methylated domains, and dynamic chromatin transitions across gestation. This configuration enables transcriptional plasticity but also creates vulnerability to maternal and environmental exposures, which can leave persistent epigenetic effects associated with fetal growth restriction, preeclampsia, preterm birth, and pregnancy loss. Placental health and disease therefore cannot be understood through protein-coding genes alone. The non-coding genome, comprising promoters, enhancers, enhancer-promoter networks, and non-coding RNAs is extensively rewired in trophoblast, with retrotransposons providing a major source of regulatory innovation. Epigenetic mechanisms coordinate these elements to establish trophoblast-specific transcriptional programs, and perturbation at any layer can disrupt differentiation, invasion, endocrine signaling, and immune modulation. Maternal inflammation, hypoxia, toxins, metabolic and psychological stress reshape epigenetically labile non-coding regions, positioning the placenta as both a developmental sensor and molecular archive of the intrauterine environment. Advances in epigenomic profiling highlight the potential of non-coding epigenetic signatures as early biomarkers, while underscoring ongoing challenges in resolving cell-type-specific regulatory programs and accurately annotating repetitive elements.

PMID:42200283 | DOI:10.1080/17501911.2026.2678924

An Integrated Strategy for Sustainable Dioxin Remediation: Sources, Places of Contamination, and Toxicity - May 27, 2026

Molecules. 2026 May 18;31(10):1705. doi: 10.3390/molecules31101705.

ABSTRACT

Dioxins are highly persistent organic pollutants that exist in soil. Their hydrophobic and lipophilic characteristics facilitate long-term stability, posing high risks to the ecosystem and human health. They can be released by different sources, such as the incineration of waste materials, industrial activities, the production of pesticides, and natural or accidental events like forest fires. Dioxins accumulate in food chains and persist in the environment because dioxins are less volatile as well as chemically stable and can strongly bind to organic matter. The accumulation and persistence of dioxins in aquatic and terrestrial systems make them a significant threat to the environment, even at very low concentrations. This review explains the key sources of dioxin-contaminated soil, including industrial emissions and atmospheric deposition, and assesses the associated risks. The transport, places of contamination, and overall status of dioxins are also highlighted in this study. The review also examines the mechanisms of dioxin toxicity, focusing on their interference with hormonal functions and gene expression, as mediated through the aryl hydrocarbon receptor (AhR). This AhR activation leads to gene responses and causes immunotoxicity, endocrine disruption, and oxidative stress. Furthermore, various remediation strategies like biological, physical, and chemical remediation are discussed here as effective approaches for reducing ecological and health risks and promoting soil sustainability.

PMID:42197259 | PMC:PMC13209661 | DOI:10.3390/molecules31101705

MicroRNA-425-3p: A Promising Biomarker and Candidate for Pharmacological Intervention in Neuropsychiatric Disabilities with Relevance to Major Depressive Disorder - May 27, 2026

Neuropsychiatr Dis Treat. 2026 May 20;22:611548. doi: 10.2147/NDT.S611548. eCollection 2026.

ABSTRACT

Major depressive disorder (MDD) affects more than 280 million people worldwide and is one of the leading contributors to disability, premature mortality, and overall disease burden. Nearly 60% of individuals who die by suicide have an MDD diagnosis, underscoring its profound impact on both individuals and society. MDD arises from a complex interplay of genetic vulnerability, life experiences, and molecular alterations. Among these, epigenetic mechanisms have received particular attention because they help explain how environmental stress-especially chronic stress-can produce enduring biological changes. MicroRNAs (miRNAs) represent a key class of epigenetic regulators. These small, noncoding RNAs influence the efficiency with which target genes are translated into protein, thereby exerting potent post-transcriptional control over gene expression. Approximately 70% of known miRNAs are expressed in the brain, where they shape neuronal development, synaptic plasticity, and stress responsivity. Dysregulation of miRNA expression can disrupt coordinated gene networks and has been repeatedly associated with impairments in neurogenesis, neurotransmission, neuroinflammation, and endocrine signaling-processes central to the pathophysiology of MDD and other stress-related psychiatric conditions. Within this broader landscape, miR-425 has emerged as a particularly relevant epigenetic regulator across several brain disorders. Alterations in miR-425 expression have been reported in individuals with stress-related conditions and in animal models of chronic stress exposure. Emerging evidence suggests that miR-425 modulates several mood-relevant pathways, including regulation of the hypothalamic-pituitary-adrenal (HPA) axis, neuronal cell death, inflammatory signaling, and antidepressant treatment response as well as key signaling networks such as MAPK and Wnt. Given its regulatory role and disease-associated expression changes, miR-425 has gained significant interest as both a biomarker and a potential therapeutic target. In this review, we examine its biogenesis, molecular targets, and translational importance, positioning miR-425 as a promising candidate for psychiatric intervention strategies. A substantial knowledge gap remains and needs further study. For example, the functions of miR-425 within specific cell types and neural circuits are less defined, and most available evidence derives from rodent studies. Also, the support for miR-425 as a biomarker needs large, standardized, multisite, longitudinal studies integrating neuroimaging, proteomics, and detailed clinical phenotyping. In addition, we are only beginning to understand how pharmacologic and lifestyle interventions influence miR-425 expression. Finally, key downstream targets of miR-425 and safe, cell-type-specific delivery approaches for miR-425-based therapeutics remain underdeveloped. Collectively, these gaps underscore the need for rigorous, multimodal, translational research to determine the potential of miR-425 as both a biomarker and a target for novel treatments.

PMID:42199924 | PMC:PMC13199736 | DOI:10.2147/NDT.S611548

Teachable Moments: Development of an Environmental Health Behavior Change Tool for Pregnant Women and Parents - May 27, 2026

Int J Environ Res Public Health. 2026 May 20;23(5):674. doi: 10.3390/ijerph23050674.

ABSTRACT

The perinatal period is a critical window of susceptibility for fetal development and awareness for women's health. Pregnant women are highly motivated to reduce environmental health risks, yet often lack personalized, actionable guidance on mitigating endocrine-disrupting chemicals and other household hazards. Grounded in Motivational Interviewing theory, a digital assessment was developed to empower parents to identify and reduce exposures. The tool screens for home-based and environmental risks across several domains: air quality, lead, tobacco, cleaning agents, pesticides, and plastics (BPA/phthalates). Based on user inputs, a defined algorithm generates a positive index score paired with prioritized, low-cost behavioral recommendations designed to shift users from risk awareness to active mitigation. Since its launch in Spring 2024, the tool has had over 1900 views. Preliminary analytics suggest promising engagement, and feedback more so suggests that the motivational-interview-based framing, which emphasizes empowerment over fear, facilitates immediate behavioral changes, such as switching to safer personal care products and improving indoor ventilation. Digital health interventions that translate complex environmental data into a single, manageable score can bridge the gap between clinical knowledge and household practice. This article details the score's calculation methodology and underlying datasets, and reports usage analytics and user feedback, discussing how digital screening can scale environmental health literacy and improve maternal and child health outcomes.

PMID:42196766 | PMC:PMC13205968 | DOI:10.3390/ijerph23050674

Exploring the Toxicological Impact of Bisphenol A on Acne Vulgaris via the PLA2G2A-Arachidonic Acid Pathway - May 27, 2026

Clin Cosmet Investig Dermatol. 2026 May 19;19:605572. doi: 10.2147/CCID.S605572. eCollection 2026.

ABSTRACT

OBJECTIVE: To investigate the potential molecular mechanisms underlying the contribution of environmental bisphenol A (BPA) exposure to acne pathogenesis, with a specific focus on the PLA2G2A-arachidonic acid pathway.

METHODS: We integrated network toxicology and machine learning to identify common target genes linking BPA exposure and acne. Core genes and key pathways were screened through differential expression, gene enrichment, and feature selection algorithms. The findings were validated in independent datasets and further investigated using immune infiltration analysis, molecular docking, and molecular dynamics simulations.

RESULTS: Three core genes were identified, with PLA2G2A being the central hub. Functional enrichment analysis revealed significant involvement of these targets in arachidonic acid metabolism, PI3K-AKT signaling, and IL-6/JAK-STAT3 pathways. PLA2G2A was upregulated in acne lesions and positively correlated with pro-inflammatory immune cell infiltration. Molecular docking and dynamics simulations indicated stable binding between BPA and PLA2G2A.

CONCLUSION: These findings suggest that BPA exposure may contribute to acne development by targeting PLA2G2A, disrupting arachidonic acid metabolism, and modulating the local inflammatory microenvironment. Crucially, this study highlights the environmental risk of endocrine-disrupting chemicals in dermatology and identifies PLA2G2A as a novel, potential therapeutic target for comprehensive acne management.

PMID:42199312 | PMC:PMC13199229 | DOI:10.2147/CCID.S605572

Gut Microbial Dysbiosis and Male Reproductive Health: Current Insights and Future Directions - May 27, 2026

Int J Mol Sci. 2026 May 16;27(10):4482. doi: 10.3390/ijms27104482.

ABSTRACT

Male infertility contributes to approximately half of all infertility cases, with a substantial proportion remaining idiopathic. Emerging evidence implicates the gut microbiome as a regulator of male reproductive health through a proposed gut-testis axis. Few studies have shown that gut microbial dysbiosis may impair sperm quality via multiple mechanisms, including disruption of endocrine function (e.g., reduced testosterone production), alterations in microbial-derived metabolites, and impaired testicular energy metabolism. Increased intestinal permeability and systemic inflammation may further compromise the blood-testis barrier, while translocation of bacterial endotoxins may also contribute to testicular damage. Collectively, these processes can disrupt spermatogenesis and negatively affect sperm parameters, such as concentration, motility, and morphology. Interventions that restore microbial balance, including dietary modulation, have shown potential in reversing these effects and improving reproductive outcomes. This review summarizes and evaluates current literature linking gut microbial dysbiosis to male reproductive dysfunction. Key methodological limitations and knowledge gaps are highlighted, providing a foundation for advancing the development of gut microbiome-based interventions to improve male reproductive health.

PMID:42196459 | PMC:PMC13207464 | DOI:10.3390/ijms27104482

Emerging Environmental Contaminants Targeting Cardiovascular Ion Channels: Exposure Effects, Underlying Mechanisms, and Implications for Cardiovascular Health Risks - May 27, 2026

Toxics. 2026 May 21;14(5):450. doi: 10.3390/toxics14050450.

ABSTRACT

PMID:42198576 | PMC:PMC13211365 | DOI:10.3390/toxics14050450

Advances in Analytical Methods for the Extraction and Quantification of Benzophenones in Breast Milk and Infant Formula: A Scoping Review and Bibliometric Analysis - May 27, 2026

Foods. 2026 May 12;15(10):1693. doi: 10.3390/foods15101693.

ABSTRACT

Benzophenones (BPs) and derivatives are endocrine-disrupting chemicals (EDCs) widely used in personal care products, food packaging, and flavoring ingredients. This systematic review and bibliometric analysis aimed to identify and summarize analytical methods used to determine BPs in human milk and infant formulas. Furthermore, the bibliometric evaluation explored publication trends by journal, citation count, and geographical distribution, providing insight into the global research landscape on this topic. The most employed sample preparation techniques included liquid-liquid extraction, solid-phase extraction, dispersive solid-phase extraction, low-temperature partitioning, QuEChERS, and dispersive liquid-liquid microextraction, frequently combined with enzymatic treatments with β-glucuronidase or arylsulfatase to improve recovery and sensitivity. Gas chromatography (GC) and liquid chromatography (LC) coupled with mass spectrometry (MS) were the predominant analytical platforms, with LC-MS being the most used for its ability to detect BPs without derivatization. Recent studies have shown a trend of replacing conventional organic solvents with greener, sustainable, and environmentally friendly approaches, such as miniaturized methods. This trend aligns with Green Analytical Chemistry principles and highlights the need for ongoing methodological and regulatory advancements to ensure food safety and protect public health.

PMID:42195897 | PMC:PMC13206393 | DOI:10.3390/foods15101693

The Toxicological Effects of Emerging Pollutants on Marine Invertebrates: A Review - May 27, 2026

Toxics. 2026 May 20;14(5):447. doi: 10.3390/toxics14050447.

ABSTRACT

Marine invertebrates are characterized by high species diversity, a wide distribution, ease of culture, low cost, short life cycles and high sensitivity to pollutants, which makes them excellent models for observing toxic effects and elucidating underlying mechanisms. This paper reviews representative species from three phyla-Arthropoda, Mollusca, and Echinodermata-under both single emerging contaminant exposure and combined exposure scenarios, and analyzes the reproductive and neurotoxic impacts of these contaminants on marine invertebrates. Neurotoxicity is mediated by several key mechanisms: inhibition of acetylcholinesterase activity; disruption of neurotransmitter balance, oxidative stress; and cellular damage, interference with embryonic neural development and axis specification, and impairment of neural cell differentiation and migration. Reproductive toxicity impairs reproductive development by disrupting endocrine signaling, inducing oxidative stress, downregulating reproduction-related genes and damaging gonadal structure. Studies have shown that, besides environmental factors, contaminant concentration is closely correlated with toxic potency and differing concentration ratios can lead to either antagonistic or synergistic effects in combined toxicity. Current research has largely focused on single or binary contaminant systems, whereas studies on multi-contaminant mixtures and their interactions with multiple environmental factors remain limited. Future research should prioritize combined exposure to multiple contaminants, long-term multigenerational observations and the development of comprehensive ecological risk assessment models and monitoring standards, thereby providing a scientific basis for marine ecological conservation.

PMID:42198573 | PMC:PMC13211650 | DOI:10.3390/toxics14050447

Protective Effects of Myrtus communis Essential Oil Against Bisphenol A-Induced Sperm Dysfunction: Insights from Lipidomic, Amino Acid Profiling, Oxidative Stress and Molecular Docking - May 27, 2026

Antioxidants (Basel). 2026 Apr 24;15(5):536. doi: 10.3390/antiox15050536.

ABSTRACT

BisphenolA (BPA) is a common endocrine disruptor that impairs male fertility through oxidative stress and alterations in membrane lipids. This study evaluated the protective effects of Myrtus communis L. essential oil (EOMC) on BPA-induced sperm toxicity in Wistar rats in vitro. BPA significantly decreased sperm motility and viability. It also increased lipid peroxidation, depleted thiols, and reduced the activity of antioxidant enzymes (SOD, CAT-like and GPx-like). Concomitant treatment with low and intermediate doses of EOMC (0.5-1 µL/mL) restored sperm function, reduced oxidative stress, and preserved membrane phospholipids. However, the highest dose (5 µL/mL) further impaired sperm function and disrupted membrane phospholipids. BPA also altered amino acid profiles and accumulated intracellularly, effects partially reversed by EOMC, which redistributed free BPA into the culture medium. Bioavailability analysis revealed selective absorption of α-pinene, while d-limonene and 1,8-cineole were undetectable. Molecular modeling indicated strong binding of BPA to antioxidant enzymes, potentially disrupting their structure and activity. Overall, these results show that EOMC protects sperm from BPA-induced damage in a dose-dependent manner through antioxidant, membrane-stabilizing, and redistribution mechanisms. This highlights its potential application in phytotherapy for male reproductive health.

PMID:42193158 | PMC:PMC13203262 | DOI:10.3390/antiox15050536

Microplastics as both a driver of genitourinary cancers and a deliverer of treatments - May 27, 2026

Commun Med (Lond). 2026 May 27;6(1):311. doi: 10.1038/s43856-026-01675-7.

ABSTRACT

PMID:42203887 | PMC:PMC13216587 | DOI:10.1038/s43856-026-01675-7

Elucidating the molecular mechanisms linking bisphenol A to breast cancer: an integrated study of bioinformatics, machine learning, and molecular docking - May 27, 2026

Naunyn Schmiedebergs Arch Pharmacol. 2026 May 27. doi: 10.1007/s00210-026-05489-1. Online ahead of print.

ABSTRACT

Bisphenol A (BPA) is a prevalent environmental endocrine disruptor linked to breast cancer. However, the precise molecular mechanisms and core therapeutic targets remain to be fully elucidated. This study employed an integrative multi-omics approach to explore the potential mechanism of BPA-associated breast cancer. We integrated multiple transcriptomic datasets from the Gene Expression Omnibus (GEO) database and identified intersection targets between BPA and breast cancer through differential expression analysis, WGCNA, and multi-source database predictions (ChEMBL, PharmMapper, SEA). Pathway enrichment analyses revealed that these targets are predominantly involved in key signaling cascades, such as MAPK and PI3K/Akt. To identify robust biomarkers, we constructed a diagnostic model using machine learning algorithms and prioritized core genes via SHapley Additive exPlanations (SHAP) value analysis. Five core genes (EGFR, PPARG, MMP12, ADRB2, and KIF11) were identified, all of which demonstrated high diagnostic accuracy (AUC > 0.7) in validation sets. Subsequent molecular docking and molecular dynamics simulations predicted that BPA exhibits strong binding affinity (binding energy < - 5 kcal/mol) to these core proteins. Collectively, our findings suggest that BPA may promote breast cancer progression by modulating these core targets and interfering with the MAPK/PI3K/Akt pathways. This study provides a data-driven theoretical basis for elucidating the molecular link between BPA and breast cancer, proposing potential biomarkers that warrant further investigation for clinical diagnosis and intervention.

PMID:42201343 | DOI:10.1007/s00210-026-05489-1

Zeolite-Based Composite Nanomaterials for Organic Micropollutant Removal: Structure-Property-Performance Relationships and Practical Challenges - May 26, 2026

Nanomaterials (Basel). 2026 May 20;16(10):635. doi: 10.3390/nano16100635.

ABSTRACT

Zeolite-based composite nanomaterials represent a versatile and mechanistically rich platform for the removal of organic micropollutants (OMPs)-including pharmaceuticals, endocrine-disrupting compounds, pesticides, and per- and polyfluoroalkyl substances (PFAS)-from contaminated water systems. Although pristine zeolite frameworks provide well-defined microporous architectures, tunable Si/Al ratios, and ion-exchange capacity, their intrinsic hydrophilicity restricts interaction diversity and limits performance toward the structurally heterogeneous OMPs prevalent in real aquatic environments. Composite integration with carbonaceous nanophases, functional polymers and surfactants, and catalytically active metal oxide nanoparticles substantially extends this interaction repertoire, yielding multifunctional materials whose adsorption performance exceeds that of the individual components. Drawing on a systematic survey of peer-reviewed literature published between 2016 and 2026, this review develops a mechanism-oriented, structure-property-performance framework examining five dominant adsorption mechanisms-electrostatic attraction, π-π stacking, hydrogen bonding, hydrophobic partitioning, and micropore confinement-in relation to composite nanoarchitecture, surface chemistry, and structural parameters. The modulating influence of realistic water matrix conditions on adsorption efficiency is critically assessed, alongside challenges of regeneration, long-term stability, metal leaching, and the persistent gap between laboratory-scale synthesis and scalable deployment. Priority research directions are identified, including standardized performance evaluation under environmentally representative conditions and rational design of hierarchical multifunctional nanocomposites from earth-abundant and waste-derived precursors.

PMID:42188530 | PMC:PMC13210204 | DOI:10.3390/nano16100635

Obesity, Low-Grade Chronic Inflammation, and Clinical Outcomes in Spondyloarthritis: A Translational Synthesis - May 26, 2026

Metabolites. 2026 May 21;16(5):347. doi: 10.3390/metabo16050347.

ABSTRACT

This translational synthesis highlights the potential role of obesity-induced low-grade chronic inflammation in modulating clinical outcomes among patients with spondyloarthritis (SpA). Obesity transforms adipose tissue into a pro-inflammatory endocrine organ, where hypertrophic adipocytes release adipokines such as leptin alongside cytokines including TNF-α and IL-6, potentially contributing to macrophage polarization toward an M1 phenotype and activating NF-κB signaling pathways. This systemic immunometabolic priming may lower activation thresholds at the enthesis-the primary pathological site in SpA-potentially amplifying IL-23/IL-17 axis activity via Th17 bias, innate-like lymphocyte responses, and stromal-immune crosstalk under mechanical stress. Clinically, patients with SpA and obesity have been reported to demonstrate heightened disease activity (BASDAI, ASDAS), impaired function (BASFI), accelerated radiographic progression (syndesmophytes, enthesophytes), and diminished biologic response rates, potentially attributable to pharmacokinetic alterations (e.g., subtherapeutic TNF inhibitor levels) and pharmacodynamic resistance. Multisystem comorbidities, including non-alcoholic fatty liver disease, cardiovascular events, metabolic syndrome, sleep disturbances, and depression, further exacerbate morbidity and diminish quality of life. Therapeutic implications emphasize obesity as a modifiable disease modifier. Weight loss interventions, including hypocaloric diets, anti-inflammatory regimens (e.g., Mediterranean diet), multicomponent exercise, GLP-1 receptor agonists, and bariatric surgery, have been associated with reductions in inflammatory biomarkers, improved remission rates (MDA, DAPSA), and prolonged drug survival by restoring adipokine balance and disrupting mechano-inflammatory loops. Future randomized controlled trials should prioritize long-term evaluations of integrated multidisciplinary strategies that combine metabolic optimization with immunomodulatory therapies, addressing adherence challenges through psychological support and patient-tailored protocols, while elucidating dose-response relationships for GLP-1RAs and exercise in diverse SpA subtypes to establish precision management paradigms that mitigate cardiometabolic burden and improve holistic outcomes.

PMID:42188056 | PMC:PMC13208230 | DOI:10.3390/metabo16050347

Dietary effects of early nutrition on muscle mass and accretion in mammals - May 26, 2026

Best Pract Res Clin Endocrinol Metab. 2026 May 7:102111. doi: 10.1016/j.beem.2026.102111. Online ahead of print.

ABSTRACT

Skeletal muscle serves as the primary protein reservoir in neonates and is a major determinant of early postnatal growth. This period features exceptionally high muscle protein synthesis, driven by increased sensitivity to feeding-induced insulin and amino acid signals that converge on the mechanistic target of rapamycin complex 1 (mTORC1). These signals regulate postnatal metabolic activation and anabolic responsiveness, rather than driving developmental transitions. This review summarizes the endocrine, nutrient-sensing, and energy-sensing pathways that regulate early-life skeletal muscle accretion, highlighting translational efficiency, ribosomal capacity, and myonuclear accretion as key determinants of growth. Evidence from translational neonatal models, particularly the pig, demonstrates coordinated control of muscle anabolism by insulin/IGF signaling, amino acid sensing, and cellular energy status, and shows how prematurity and intrauterine growth restriction disrupt these processes, resulting in anabolic resistance. Colostrum and milk support muscle growth primarily by enhancing intestinal maturation, nutrient delivery, and postprandial endocrine responses, whereas direct programming via milk-derived extracellular vesicles remains uncertain.

PMID:42191489 | DOI:10.1016/j.beem.2026.102111

Effects of Zearalenone on the Kiss1/GPR54 System and Related Genes Expression in the Hypothalamus and Pituitary Gland of Weaned Gilts - May 26, 2026

Toxins (Basel). 2026 Apr 22;18(5):195. doi: 10.3390/toxins18050195.

ABSTRACT

Zearalenone (ZEA) is a potent estrogenic mycotoxin known to disrupt reproductive functions, but its precise central neuroendocrine mechanisms remain unclear. This study investigated the effects of ZEA on the hypothalamic-pituitary Kiss1/GPR54 signaling pathway in weaned gilts. A total of 32 gilts were randomly assigned to four dietary treatments contained with 0, 0.15, 1.5, or 3.0 mg/kg ZEA for a 32-day feeding trial. Histopathology, immunohistochemistry, and mRNA/protein expression analyses of GPR30, Kiss1, GPR54, GnRH, and GnRHR in the hypothalamus and pituitary gland were conducted. ZEA exposure induced significant histological damage in both tissues. In the hypothalamus, Kiss1, GPR54, GnRH, and GnRHR exhibited a non-linear response, increasing at moderate doses and decreasing at 3.0 mg/kg ZEA, whereas GPR30 expression was continuously upregulated. In the pituitary gland, GnRHR showed a similar non-linear pattern. Furthermore, high-dose ZEA down-regulated pituitary Kiss1 and GPR54 while up-regulating GnRH and GPR30 expressions. In conclusion, ZEA induces reproductive neuroendocrine toxicity through a complex, dose-dependent modulation of the Kiss1/GPR54 signaling axis. The persistent upregulation of GPR30 suggests it acts as a crucial mediator in disrupting this endocrine feedback loop within the hypothalamus and pituitary gland.

PMID:42188598 | PMC:PMC13211516 | DOI:10.3390/toxins18050195

Comprehensive Insight into the Male Dog Reproductive System in Health and Diseases: Developmental, Genetic, and Environmental Factors-Review on Research and Clinical Trials - May 26, 2026

Vet Sci. 2026 May 11;13(5):464. doi: 10.3390/vetsci13050464.

ABSTRACT

As in other mammalian species, the complex and specific interactions between internal biological processes and external factors regulate and impact the male dog reproductive system functions. This comprehensive review integrates physiological and molecular mechanisms underlying the reproductive system maintenance throughout the anatomical and histological structure of reproductive organs and their functions from development to aging. Simultaneously, the presentation of fundamental hormonal regulations and functions of the reproductive system is comprised. Special attention is put on e.g., genetic, developmental, age- and environmental-related disorders. The structural and hormonal status of the reproductive organs in response to single or mixed influences: genetic predispositions (e.g., cryptorchidism, sex chromosome aneuploidy syndrome), developmental courses (e.g., cryptorchidism, uterus masculinus, hypospadias), age-related diseases (e.g., tumors), and environmental stressors: e.g., endocrine-disrupting chemicals, toxins, heat stress (possibly leading to e.g., hypogonadism, cryptorchidism, infertility, tumors, precocious aging) is provided. Such multidirectional and comprehensive associations of grouped, selected, clinically significant pathological processes and diseases are broadly considered and linked here for the first time. Based on both epidemiological and experimental findings, the etiologies, current diagnostic approaches, treatment options, and prognostic assessments of these common male dog disorders are presented. This compendium seems useful for young veterinarians, researchers, breeders, and dog owners, enabling them to integrate knowledge on biological principles and processes with clinical practices and research in recent and future canine andrology.

PMID:42188934 | PMC:PMC13211336 | DOI:10.3390/vetsci13050464

Reframing Heart Failure as a Multiorgan Network Disorder: Translational and Regenerative Perspectives in Veterinary Cardiology - May 26, 2026

Vet Sci. 2026 Apr 29;13(5):435. doi: 10.3390/vetsci13050435.

ABSTRACT

Heart failure (HF) has traditionally been regarded as a primary myocardial disorder in veterinary medicine. However, accumulating evidence suggests that HF represents a systemic syndrome characterized by dynamic multiorgan interactions. In human cardiovascular research, cardiorenal and cardiointestinal paradigms have reshaped disease conceptualization, yet comparable integrative frameworks remain underdeveloped in veterinary cardiology. Naturally occurring canine HF-particularly myxomatous mitral valve disease and dilated cardiomyopathy-offers a clinically relevant translational platform in which systemic remodeling unfolds within an intact physiological lifespan. This review proposes a systems-based perspective that integrates spontaneous canine HF with controlled in vivo experimental models. We outline four main pathways of interaction: (1) the heart-gut axis, wherein reduced perfusion can influence inflammation and disruption of the intestinal barrier; (2) the heart-bone axis, wherein endocrine factors like osteoprotegerin and osteocrin can impact remodeling of the cardiovascular system; (3) the heart-vascular endothelium axis, wherein inflammatory signaling and dysfunction of the vascular endothelium are hallmarks; and (4) the neurocardiac axis, which reflects an imbalance in the autonomic nervous system. Emerging regenerative and organelle-based strategies-including mesenchymal stem cell therapy and mitochondrial transplantation-are discussed within this multiorgan framework. Rather than focusing solely on cardiac contractility, these approaches may function as systemic inflammatory modulators, and endothelial, metabolic, and autonomic pathways. Canine HF can be better understood as a multiorgan network condition; reframing it in this way can help researchers in the field of translational cardiology create more comprehensive diagnostic and treatment plans.

PMID:42188906 | PMC:PMC13211417 | DOI:10.3390/vetsci13050435

Hydrophobic Tag Degraders Overcome Endocrine-Resistant Breast Cancer by Recruiting HSP27-Mediated E3 Ligase Complex for ERalpha Proteasomal Degradation - May 26, 2026

Angew Chem Int Ed Engl. 2026 May 26:e25741. doi: 10.1002/anie.202525741. Online ahead of print.

ABSTRACT

Hydrophobic tag (HyT)-mediated protein degradation has emerged as a pivotal tool for targeted protein degradation (TPD), yet its underlying degradation mechanism remains incompletely elucidated. Herein, we designed structurally optimized HyT-based degraders by covalently conjugating hydrophobic amino acid tags to ERα-targeting ligands via alkane linkers of varying lengths, identifying the lead compound VI-10h. VI-10h exhibited potent antiproliferative activity and efficient ERα degradation in endocrine-resistant breast cancer cells (LCC2, MCF-7^D538G, MCF-7^Y537S, and MCF-7^EGFR) and superior antitumor activity compared to the clinical drug fulvestrant (Ful) in MCF-7 and tamoxifen-resistant LCC2 xenograft models. To elucidate the HyT-mediated degradation mechanism, we synthesized biotin-conjugated HyTs (biotin-Lys and biotin-Trp) and performed pull-down assays combined with mass spectrometry. Our results unveiled that VI-10h selectively recruits heat shock protein 27 (HSP27) as a non-canonical E3 ligase adaptor protein, forms an ERα-HSP27-RING1 ternary complex to promote ERα degradation, disrupts estrogen-dependent oncogenic networks, and circumvents the drug resistance associated with conventional CRBN- or VHL-dependent E3 ligase-recruiting degraders. This study clarifies a HyT-mediated ERα degradation mechanism and supports the feasibility of using HyT degraders to overcome resistance to conventional E3 ligase-recruiting strategies and endocrine-resistant breast cancer, thereby establishing a molecular design strategy for next-generation targeted degraders.

PMID:42189698 | DOI:10.1002/anie.202525741

Zeolite-Based Composite Nanomaterials for Organic Micropollutant Removal: Structure-Property-Performance Relationships and Practical Challenges - May 26, 2026

Nanomaterials (Basel). 2026 May 20;16(10):635. doi: 10.3390/nano16100635.

ABSTRACT

PMID:42188530 | PMC:PMC13210204 | DOI:10.3390/nano16100635

Effects of norgestrel on the reproductive endocrine system, hepatic damage and antioxidant responses of marine medaka (Oryzias melastigma) at different salinities - May 26, 2026

Aquat Toxicol. 2026 May 18;297:107865. doi: 10.1016/j.aquatox.2026.107865. Online ahead of print.

ABSTRACT

Norgestrel, a widely used synthetic progestin, may threaten marine ecosystems, although research on its impact is limited. In this study, marine medaka (Oryzias melastigma) embryos were exposed to combinations of two salinity levels (30 ‰, 10 ‰) and three norgestrel concentrations (0, 3.69, 17.96 ng/L; 0, 3.76, 18.41 ng/L) for 90 days until adulthood, and the effects on growth, sex differentiation, reproduction, liver health, and antioxidant responses were evaluated. Results showed that low salinity reduced growth, whereas norgestrel did not significantly affect growth at either salinity. However, high norgestrel concentration reduced egg production, induced a male-biased sex ratio, and caused histopathological changes such as fibrosis and reduced sperm count in testicular tissue, irregular oocyte morphology, and even the presence of bisexual structures at both salinities. In females, norgestrel lowered FSH, LH, and T levels but increased E2 and 11-KT across both salinity conditions. Norgestrel under low or high salinity altered gene expression in gonads: it up-regulated erα, erβ, lhr, star, cyp11a, 3βhsd, cyp17a1, and cyp19a genes in females, but down-regulated erα, erβ, fshr, lhr, star, cyp11a, 3βhsd, cyp17a1, 17βhsd, cyp11b, cyp19a and pgr genes in males. In male liver tissues, norgestrel increased expression of erα, arα, vtg1, vtg2, chgh, and chgl genes under high salinity. These gene transcriptional alteration and reproductive hormonal imbalances, ultimately reduced egg production. Norgestrel also induced liver damage at both salinities, more severely in females. Additionally, norgestrel lowered CAT activity in ovaries, suggesting ovarian damage. Two-way ANOVA revealed a significantly interaction between salinity and norgestrel, indicating that salinity modulates norgestrel's toxic effects on sexual differentiation, egg production, reproductive hormones, gene transcription, and oxidative stress. In contrast, norgestrel's effects on growth, gonadal and hepatic histology were independent of salinity. Principal component analysis (PCA) further validated the overall disruptive effects of salinity and NGT, showing clear separation between treatment groups driven by HPG axis-related genes, reproductive hormones, and growth traits. This study highlights the reproductive endocrine-disrupting potential of norgestrel in coastal environments with variable salinity.

PMID:42190302 | DOI:10.1016/j.aquatox.2026.107865

17β-estradiol reshapes the reproductive dose-response to polystyrene nanoplastics in the rotifer Brachionus calyciflorus - May 26, 2026

Aquat Toxicol. 2026 May 21;297:107869. doi: 10.1016/j.aquatox.2026.107869. Online ahead of print.

ABSTRACT

Nanoplastics (NPs) sorb co-occurring contaminants, yet how endocrine-disrupting chemicals condition NP toxicity remains poorly resolved. Using the freshwater rotifer Brachionus calyciflorus, we combined a full-factorial design of 70 nm polystyrene NPs and 17β-estradiol (E2) with a focused NP concentration gradient under a fixed E2 background of 300 μg L^-1. Two-way ANOVA revealed significant E2 × NPs interactions for lifespan, total offspring, and final population density, indicating background-dependent NP effects. At E2 = 300 μg L^-1, low-dose NPs (1 μg mL^-1) increased total offspring by 18.29 % relative to E300N0, whereas 5 μg mL^-1 decreased total offspring by 32.20 %, producing a non-monotonic dose-response curve. A Gaussian fit located the stimulation peak at 1.11 μg mL^-1 and an approximate transition point at 2.50 μg mL^-1. Corrected relative internal fluorescence during 0-4 h post-transfer was higher in E300N5 than in N5. Oil Red O staining and triglyceride assays indicated neutral lipid depletion across treatments, and qPCR showed tor downregulation specific to E300N5, alongside suppression of rar/rxr and the reproduction-related markers vasa and nanos. Collectively, these findings identify endocrine background as a state variable capable of reshaping nanoplastic reproductive toxicity, with implications for mixture-risk assessment in aquatic invertebrates.

PMID:42190301 | DOI:10.1016/j.aquatox.2026.107869

Quercetin Reverses DEHP-Induced ZBP1-Mediated PANoptosis in Thymus by Targeting NF-κB to Regulate the TNF-α/ROS Signaling Pathway - May 26, 2026

J Nutr Biochem. 2026 May 25:110423. doi: 10.1016/j.jnutbio.2026.110423. Online ahead of print.

ABSTRACT

Quercetin (Que), a natural dietary flavonoid, possesses significant antioxidative and immunoregulatory properties. Di(2-ethylhexyl) phthalate (DEHP), a pervasive environmental endocrine-disrupting chemical, triggers oxidative stress (OS) and elicits immunotoxic effects in various species. However, whether Que can target NF-κB to alleviate DEHP-induced OS and PANoptosis in the chicken thymus remains unclear to date. To investigate the mechanism of thymus damage induced by DEHP and the intervention effect of Que, we established an in vivo chicken model treated with DEHP and/or Que. Based on the results of network pharmacology, molecular docking, molecular dynamics simulations, and Cell Thermal Shift Assay (CETSA), we predicted that NF-κB is the key target for the protective effect of Que. Subsequently, through H&E staining, CCK-8, immunofluorescence, Western blot and other techniques, we verified the effects of DEHP and/or Que on OS, the assembly of PANoptosome, and cellular PANoptosis in chicken thymus tissue and chicken lymphocyte cell line (MSB-1). Meanwhile, to clarify the key role of NF-κB in the above regulatory process, we conducted reverse validation experiments by introducing the NF-κB activator Act1 in cellular experiments. The results demonstrated that DEHP exposure markedly induces the upregulation of NF-κB and TNF-α(P<0.05), leading to a pronounced burst of reactive oxygen species (ROS) and consequent OS within the chicken thymus. This process further activates the ZBP1-mediated PANoptosis pathway, ultimately causing damage to chicken thymus tissue. Que intervention effectively suppresses NF-κB activation, blocking the transmission of the NF-κB/TNF-α/ROS signaling axis, thereby reversing DEHP-induced ZBP1-mediated PANoptosis in chicken thymus.

PMID:42191001 | DOI:10.1016/j.jnutbio.2026.110423

Effects of tributyltin as an obesogen chemical on mammalian adipose tissue - May 26, 2026

Mol Cell Endocrinol. 2026 May 25:112833. doi: 10.1016/j.mce.2026.112833. Online ahead of print.

ABSTRACT

Tributyltin (TBT) is an endocrine-disrupting chemical (EDC) with well-established obesogenic properties, promoting adipogenesis and disrupting metabolic homeostasis, thereby contributing to obesity. Owing to its high lipophilicity, TBT readily bioaccumulates through aquatic and terrestrial food chains. Because of these physicochemical characteristics and its environmental persistence, TBT remains detectable worldwide, despite the global ban on its use in antifouling paints implemented in 2008. The obesogenic activity of TBT is primarily mediated through the activation of peroxisome proliferator-activated receptor gamma (PPARγ) and retinoid X receptor (RXR), key regulators of adipocyte differentiation and lipid metabolism. This review includes original research articles focusing on the effects of TBT on adipose tissue. Evidence indicates that TBT induces upregulation of adipogenic markers in white adipose tissue (WAT), impairs thermogenic capacity in brown adipose tissue (BAT), and suppresses the browning process of WAT. Additionally, TBT modulates estrogen-responsive gene expression in pink adipose tissue (PAT). Notably, these effects have been reported at environmentally relevant, low-dose exposures, underscoring TBT as persistent public health concern and highlighting the need for further epidemiological studies and investigations of human exposure. This review integrates evidence from in vitro models, in vivo mammalian studies, and human data, and identifies critical gaps in the current literature, proposing future research directions to elucidate the molecular mechanisms underlying TBT-induced toxicity in adipose tissues.

PMID:42191116 | DOI:10.1016/j.mce.2026.112833

Upcycling shaddock peel waste into a Fe/Fe3C@porous carbon sensor for ultrasensitive electrochemical detection of carbendazim - May 26, 2026

Anal Chim Acta. 2026 Aug 1;1409:345603. doi: 10.1016/j.aca.2026.345603. Epub 2026 Apr 30.

ABSTRACT

BACKGROUND: Pesticide residues in foods, particularly carbendazim, a widely used fungicide associated with endocrine disruption and genotoxicity, pose significant health risks even at trace levels. The complexity of food matrices necessitates the development of highly sensitive, selective, and sustainable detection methods for routine food safety monitoring.

RESULTS: Here, Fe/Fe₃C nanoparticles-decorated porous carbon composite (Fe/Fe₃C@PC) was prepared via facile in-situ iron doping and one-step carbonization strategy by using the agricultural waste (shaddock peel) as the precursor. The as-synthesized Fe/Fe₃C@PC exhibits enlarged electroactive surface area, accelerated electron transfer, and remarkable adsorptive affinity for carbendazim. Density functional theory (DFT) calculations elucidate this enhanced affinity, revealing that while the carbon matrix provides moderate adsorption via π-π stacking, the embedded Fe and Fe₃C nanoparticles introduce stronger coordination interactions, creating a synergistic interface that enriches the target analyte. Based on the excellent physicochemical property of Fe/Fe₃C@PC, a novel electrochemical sensor was fabricated, and the optimized sensor demonstrates outstanding analytical performance with a wide linear range (1 nM to 1 μM) and an ultra-low detection limit of 0.25 nM. When applied to real food samples, the sensor successfully quantified carbendazim in spiked tea and juice samples, achieving satisfactory recoveries between 90.5% and 97.4%.

SIGNIFICANCE: This work provides a sustainable valorization pathway for biomass waste while establishing a highly sensitive and reliable platform for routine fungicide monitoring. The successful validation in complex food matrices demonstrates its practical potential for safeguarding consumer health and advancing food safety control.

PMID:42191307 | DOI:10.1016/j.aca.2026.345603

Effects of White Bualuang (Nelumbo nucifera Gaertn.) Extract on Testicular Histomorphometry and Spermatogenic Parameters in Mancozeb-Exposed Rats - May 26, 2026

Biology (Basel). 2026 May 7;15(10):738. doi: 10.3390/biology15100738.

ABSTRACT

Male infertility is an increasing global health concern associated with declining population growth. Mancozeb (MZ) exposure may induce reproductive toxicity through endocrine disruption and oxidative stress, impairing spermatogenesis. This study evaluated the effects of White Bualuang extract (WBE) on sexual behavior, testicular histomorphometry, and spermatogenic parameters in rats exposed to MZ. Thirty mature male rats were randomly assigned to the following five groups (n = 6): Control, MZ 500 mg/kg, MZ + 0.55 mg/kg WBE, MZ + 1.10 mg/kg WBE, and MZ + 2.20 mg/kg WBE, for 30 days. Sexual behaviors, relative testis weight, antioxidant properties, and histomorphometry parameters were determined. MZ-exposed rats had significantly decreased courtship behavior, seminiferous tubule diameter, and a tendency toward decreased spermatogenic cell numbers, along with enlarged interstitial spaces. However, pretreatment with WBE, especially at a dose of 0.55 mg/kg, showed improvements in courtship behavior and several histomorphometry parameters and was associated with increased Sertoli cell efficiency and spermatogenic organization compared with the MZ group. WBE showed potential to reduce lipid peroxidation (LPO) and advanced oxidation protein products (AOPP) in MZ-exposed rats, particularly, the 0.55 mg/kg dose improved courtship behavior and reproductive parameters, supporting further investigation of WBE as an antioxidant and potential functional supplement.

PMID:42187700 | PMC:PMC13203518 | DOI:10.3390/biology15100738

Toxoplasma gondii as a Direct Cause of Reproductive Dysfunction: Dual Threats to Male and Female Fertility - May 26, 2026

Vet Sci. 2026 Apr 28;13(5):430. doi: 10.3390/vetsci13050430.

ABSTRACT

Toxoplasma gondii, an obligate intracellular protozoan infecting approximately one-third of the global population, poses a significant yet underappreciated threat to reproductive health in both sexes. Although this parasite has long been linked to birth defects caused by infection during pregnancy, new research shows that it also reduces fertility in both sexes through different but related mechanisms. This review synthesizes knowledge on T. gondii-induced reproductive pathology across females and males, examining shared mechanistic themes while respecting tissue-specific differences, and evaluates emerging therapeutic strategies. In females, the parasite establishes persistent uterine reservoirs, triggers decidual immune dysregulation characterized by NK cell cytotoxicity, M1 macrophage polarization, Treg apoptosis, and inflammasome-mediated pyroptosis, while disrupting estrogen and progesterone signaling through both host receptor modulation and intrinsic parasite steroidogenic enzymes (TgCYP450mt, TgMAPR, Tg-HSD). In males, T. gondii breaches the blood-testis barrier, induces germ cell and Leydig cell apoptosis via ER stress and caspase pathways, impairs sperm quality parameters across acute and chronic infection, and disrupts the hypothalamic-pituitary-gonadal axis. Conserved molecular mechanisms-including NLRP3 inflammasome activation, PERK/eIF2α/ATF4/CHOP-mediated ER stress, and oxidative stress-operate in both reproductive tissues. The parasite's intrinsic steroidogenic capability and bidirectional hormonal manipulation represent a paradigm shift in understanding host-parasite interactions. Conventional antiparasitics face limitations due to poor reproductive sanctuary penetration. Immunomodulatory approaches targeting Trem2, Tim-3, and the NLRP3 inflammasome show promise, along with natural products including Inonotus obliquus polysaccharide and ginseng polysaccharide. Nanomedicine platforms and mRNA vaccine candidates offer new directions for overcoming tissue barrier limitations. Toxoplasma gondii represents a fundamental threat to fertility and pregnancy outcomes rather than merely a risk for congenital infection. Integrated therapeutic strategies addressing direct parasitism, immunopathology, and endocrine disruption are needed. Longitudinal cohort studies, strain-specific mechanistic comparisons, and clinical trials of immunomodulatory adjuncts are urgently required.

PMID:42188900 | PMC:PMC13211466 | DOI:10.3390/vetsci13050430

Occurrence of parabens in aquatic environments and sediments and efficiency of wastewater treatment plants in parabens removal - May 26, 2026

Sci Rep. 2026 May 26. doi: 10.1038/s41598-026-55348-5. Online ahead of print.

ABSTRACT

Parabens are endocrine-disrupting chemicals, and their entry into the human body via water sources has adverse effects on human health. In the present study, the occurrence of methylparaben, ethylparaben, propylparaben, and butylparaben in three domestic, hospital, and industrial wastewater treatment plants, and in river water and sediments, was investigated. The samples were concentrated via solid-phase extraction and analyzed by high-performance liquid chromatography. Results showed that the recovery percentage for all examined parabens was within the acceptable range of 97.4% to 103.6%, and the highest paraben concentrations were observed in influents from the hospital wastewater treatment plant (methylparaben: 34.4 ± 3.6 µg/L; propylparaben: 30.9 ± 5.4 µg/L). The study indicated that processes used in wastewater treatment plants are unable to completely remove parabens; however, the anaerobic-anoxic-aerobic process has the highest efficiency for paraben removal. The anaerobic-anoxic-aerobic process's efficiency for removing methylparaben, ethylparaben, propylparaben, and butylparaben was 72.24%, 78.37%, 79.57%, and 72.99%, respectively. Based on the results, the anaerobic-anoxic-aerobic process can be used as a primary treatment to reduce the concentration of emerging contaminants in wastewater. Given the health effects of parabens, future studies should investigate processes capable of completely removing emerging pollutants such as parabens from aquatic environments.

PMID:42192154 | DOI:10.1038/s41598-026-55348-5

Immunometabolic mechanisms of osteosarcopenic obesity: chronic inflammation, trained immunity, and systemic immune dysregulation - May 25, 2026

Front Immunol. 2026 May 7;17:1808488. doi: 10.3389/fimmu.2026.1808488. eCollection 2026.

ABSTRACT

Osteosarcopenic obesity (OSO)-the co-occurrence of osteoporosis/osteopenia, sarcopenia, and excess adiposity-is increasingly recognized in ageing populations and is strongly linked to frailty, fractures, disability, and cardiometabolic complications. However, heterogeneous operational definitions and population-specific cut-offs complicate risk stratification and mechanistic inference. Here, we propose a systems immunometabolic framework to explain coordinated deterioration of adipose tissue, skeletal muscle, and bone, focusing on chronic low-grade inflammation, trained immunity (innate immune memory), and senescence-associated signaling. Dysfunctional visceral adipose tissue emerges as an immune-active endocrine organ that sustains low-grade systemic inflammation through release of cytokines, adipokines, lipotoxic mediators, and damage-associated molecular patterns. A key mechanism potentially underpinning inflammatory persistence is trained immunity-epigenetic and metabolic reprogramming of innate immune cells and their progenitors-which establishes maladaptive inflammatory memory and amplifies inter-organ immune crosstalk. In skeletal muscle, this pro-inflammatory milieu promotes catabolic signaling and anabolic resistance, including NF-κB activation and mTOR pathway dysregulation, thereby driving impaired proteostasis, fibrosis, and fatty infiltration. In bone, inflammatory and senescence-associated signals converge on osteoclastogenic pathways and disrupt the receptor activator of nuclear factor-κB ligand (RANKL)/osteoprotegerin (OPG) axis, leading to uncoupled bone remodeling and net bone loss. Collectively, we argue that OSO can be conceptualized as a fat-initiated, system-level immunometabolic remodeling process across the adipose-muscle-bone axis. This framework supports stratified, multimodal interventions combining lifestyle modification with mechanism-based anti-inflammatory and anti-resorptive therapies, while immuno-epigenetic and senescence-targeted approaches warrant further study. Notably, OSO-specific longitudinal and interventional evidence integrating immune phenotyping and multi-omics remains limited and is needed to test causality and validate actionable biomarkers and targets.

PMID:42183270 | PMC:PMC13189923 | DOI:10.3389/fimmu.2026.1808488

Soil health to human health: impacts of soil contaminants on cardio-neurological health and clinical outcomes: a narrative review - May 25, 2026

Front Cardiovasc Med. 2026 May 7;13:1647648. doi: 10.3389/fcvm.2026.1647648. eCollection 2026.

ABSTRACT

The nexus between soil health and human health represents a critical yet underexplored dimension of cardio-neurological disease research. Soil constitutes the primary ecological substrate determining food quality, nutrient density, and ultimately nutrition security. However, progressive soil degradation and contamination by heavy metals, pesticide residues, persistent organic compounds, and microplastics within agricultural systems and the human food chain have reshaped disease risk profiles. Despite extensive investigation of air and water pollution, the intersection between soil contaminants and cardiovascular and neurological outcomes remains comparatively undercharacterized, revealing a significant knowledge gap between environmental and clinical medicine. Mechanistically, chronic ingestion of soil-derived toxicants promotes oxidative stress, mitochondrial dysfunction, endothelial injury, and neuroinflammation, while disrupting calcium signaling, lipid metabolism, and vascular autoregulation. Fertilizers, animal waste, pesticides, and organic pollutants function as endocrine-disrupting chemicals, activating the aryl hydrocarbon receptor (AhR) to mimic or impair normal endocrine and ligand signaling. In parallel, depletion of essential micronutrients from degraded soils reduces antioxidant capacity and impairs cardiometabolic and neuronal resilience. This dual burden of toxic exposure and diminished nutritional protection provides a plausible pathophysiologic framework linking contaminated soils to hypertension, atherosclerosis, ischemic stroke, cognitive impairment, and neurodegenerative processes, thereby influencing both acute and long-term clinical outcomes. From a public health perspective, compromised soil quality undermines nutrition security even where caloric supply is sufficient, subtly amplifying chronic disease risk at the population level. Hence, the integrative paradigm of healthy soil, healthy food, healthy people, and healthy planet highlights the necessity of transdisciplinary research, improved soil stewardship, and preventive strategies that recognize soil ecosystems as upstream determinants of human cardio-neurological health. Bridging the soil-to-heart-and-brain continuum offers transformative potential for precision prevention and sustainable global health, enabling earlier prevention, more precise dietary guidance, and evidence-based policies.

PMID:42181637 | PMC:PMC13189916 | DOI:10.3389/fcvm.2026.1647648

Brain Serotonin Deficiency Impairs Ovarian Reserve Function via the Hypothalamic-Pituitary-Ovarian Axis - May 25, 2026

Neurosci Bull. 2026 May 25. doi: 10.1007/s12264-026-01636-z. Online ahead of print.

ABSTRACT

Brain-derived serotonin (5-HT) is a key neurotransmitter that regulates diverse central and peripheral physiological processes, including endocrine function, mood, and circadian rhythms. Patients with anxiety and depression often exhibit reduced brain 5-HT levels, which contribute significantly to female infertility. However, the role of brain-derived 5-HT in maintaining ovarian reserve function remains unclear. We generated brain-specific Tph2 conditional knockout (Tph2-CKO) mice lacking 5-HT and observed reduced follicle numbers and anti-Müllerian hormone (AMH) levels, indicating diminished ovarian reserve (DOR). Mechanistically, Brain-derived 5-HT deficiency suppressed ovarian mTOR signaling, triggering excessive autophagy, mitochondrial dysfunction, and apoptosis. In the hypothalamus, reduced central 5-HT levels downregulated 5-HT receptor 7 (HTR7)-cAMP/PKA signaling, disrupted circadian rhythms, and decreased gonadotropin-releasing hormone (GnRH) expression, impairing hypothalamic-pituitary-ovarian (HPO) axis function. Ovarian follicle-stimulating hormone receptor (FSHR) and luteinizing hormone receptor (LHR) levels decreased, ultimately leading to DOR. Thus, 5-HT deficiency in the dorsal raphe nucleus disrupts the HPO axis via HTR7, leading to DOR.

PMID:42184065 | DOI:10.1007/s12264-026-01636-z

Microplastics and the Endocrine-Metabolic Interface: Novel Diagnostic Tools Targeting Thyroid-Adipose Axis - May 25, 2026

Environ Toxicol. 2026 May 25. doi: 10.1002/tox.70129. Online ahead of print.

ABSTRACT

Microplastics (MPs) have been identified as major environmental contaminants that can affect organisms directly and act as carriers of particles and chemical additives, thereby aggravating endocrine networks that coordinate metabolic homeostasis. However, evidence suggests that MPs and their chemical additives interfere with thyroid hormone signaling, adipocyte differentiation, and adipokine secretion. The mechanistic link across the thyroid-adipose axis remains poorly defined. This review delves into cutting-edge diagnostic technologies that are improving the identification, mapping, and understanding of MP-induced endocrine and metabolic issues. Quantum-dot nanosensors, single-cell multiomics, machine learning-assisted endocrine profiling, and microfluidic organ-on-chip systems offer high-resolution insights into how MPs interact with thyroid follicular cells and adipose tissues. These platforms, which combine environmental analysis and endocrine testing, enable the measurement of MP levels, the detection of hormone-receptor changes, and the modeling of endocrine system disruptions, facilitating the early identification of imbalances, novel treatments, and monitoring strategies. This review affirms the importance of studying thyroid toxicity with a focus on the adipose axis, emphasizing the importance of developing advanced diagnostic tools to assess metabolic risk in contaminated populations.

PMID:42179301 | DOI:10.1002/tox.70129

Soil health to human health: impacts of soil contaminants on cardio-neurological health and clinical outcomes: a narrative review - May 25, 2026

Front Cardiovasc Med. 2026 May 7;13:1647648. doi: 10.3389/fcvm.2026.1647648. eCollection 2026.

ABSTRACT

PMID:42181637 | PMC:PMC13189916 | DOI:10.3389/fcvm.2026.1647648

Clinico-behavioral, hepato-renal, erythrocytic, and genotoxicity induced by sub-chronic oral doses of acetochlor in male Japanese quail - May 25, 2026

Poult Sci. 2026 May 1;105(9):107059. doi: 10.1016/j.psj.2026.107059. Online ahead of print.

ABSTRACT

Acetochlor is one of the well-known and frequently used herbicides that acts as a potent endocrine disruptor. Still, there is a scarcity of studies examining the adverse effects of acetochlor on birds. Therefore, this study evaluated the behavioral alterations, oxidative stress, antioxidant enzymes, genotoxicity and histopathological impacts of subchronic oral doses of acetochlor in quails. A total of 80 male quails were procured and reared in four groups (A-D) for 45 days. Group A served as the control, while the birds reared in groups B, C and D received 20 mg/kg, 30 mg/kg and 40 mg/kg acetochlor on daily basis, respectively, for 45 days. Different clinical and behavioral signs were observed in quails exposed to higher doses of acetochlor. The quantity of antioxidant enzymes, including superoxide dismutase (SOD), reduced glutathione (GSH), and catalase (CAT), was significantly reduced (P < 0.05) in treated birds compared to normal/untreated birds. The values of oxidative stress parameters like lipid peroxidase (LPO) increased significantly (P ≤ 0.05) in the liver of Japanese quails exposed to higher concentrations of acetochlor. Significantly (P ≤ 0.05) increased values of DNA damage in isolated hepatocytes, enterocytes, and cells of the kidneys were recorded in acetochlor-treated quails. Results on the formation of micronuclei in erythrocytes revealed significantly (P ≤ 0.05) higher percentile rate in birds treated with higher concentrations of herbicide compared to untreated birds. At the histopathological level, various microscopic lesions like necrosis, disorganization, and disruption of hepatic cords in the liver, degeneration of renal tubular cells, widening of urinary space, necrosis of renal tubules in the kidneys, and degeneration and depletion of splenic cells in the spleen of quails were examined. The results of this research highlighted that Acetochlor induces different pathological ailments in Japanese quail even at sub-chronic oral doses.

PMID:42184636 | DOI:10.1016/j.psj.2026.107059

Ascorbic acid attenuates lead-induced oxidative stress and testosterone suppression in male Wistar rats - May 25, 2026

J Basic Clin Physiol Pharmacol. 2026 May 26. doi: 10.1515/jbcpp-2026-0042. Online ahead of print.

ABSTRACT

OBJECTIVES: Lead (Pb) exposure is a major environmental risk factor for male reproductive dysfunction, primarily mediated through oxidative stress and endocrine disruption. This study evaluated the effects of lead acetate on testicular antioxidant status and serum testosterone levels and investigated the ameliorative role of ascorbic acid (AA) in adult male Wistar rats.

METHODS: Thirty-five male Wistar rats were randomly assigned to seven groups (n=5): control, low- and high-dose lead (100 and 200 mg/kg), lead plus AA cotreatment, and withdrawal groups. Testicular antioxidant enzymes (SOD, CAT, GPx), reduced glutathione (GSH), and malondialdehyde (MDA) were assessed spectrophotometrically. Serum testosterone was measured using enzyme immunoassay. Data were analyzed using one-way ANOVA (p<0.05).

RESULTS: Lead exposure significantly increased MDA levels and reduced antioxidant enzyme activities and testosterone concentrations in a dose-dependent manner (p<0.05). Ascorbic acid coadministration significantly restored antioxidant status, elevated GSH levels, reduced lipid peroxidation, and improved testosterone levels compared with lead-only and withdrawal groups.

CONCLUSIONS: Lead acetate induces oxidative and endocrine disturbances in testicular tissue. Ascorbic acid effectively mitigates lead-induced reproductive toxicity by preserving antioxidant defenses and maintaining testosterone homeostasis.

PMID:42185232 | DOI:10.1515/jbcpp-2026-0042