Search Results (861)

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. Full article

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. Full article

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. Full article

Tequila is frequently stored or aged in polymer containers and oak casks, which can enable the migration of phthalates such as di-(2-ethylhexyl) phthalate (DEHP), an endocrine-disrupting chemical. We quantified DEHP in tequila (55% ethanol) stored in LDPE tanks, HDPE jerry cans, PET carboys, and French oak casks with and without thermal treatment during long-term storage/aging (up to 18 and 11 months, respectively). Monthly samples were extracted and analyzed by GC–MS. Migration kinetics were evaluated using empirical exponential/sigmoidal models and an analytical solution of Fick’s second law for a semi-infinite slab. In plastics, DEHP increased nonlinearly and was best described by a modified Gompertz model, exhibiting a lag phase up to 42 days (~month 2), maximum transfer rates (Rmax) up to 0.82 µg L⁻¹ day⁻¹, and late-time concentrations near 120 µg L⁻¹. The non-toasted oak cask previously used for wine showed exponential behavior, reaching ~185 µg L⁻¹ and fitting the Minchev–Minkov model, whereas the toasted cask showed minimal transfer. Although concentrations remained below a reference safety limit (1500 µg kg⁻¹), the results indicate that food-contact plastics and commonly used oak casks are not risk-free under prolonged contact, supporting model-based forecasting for quality control. Full article

Bisphenol A (BPA) is a widespread endocrine disruptor that interferes with metabolism in humans and animals by inducing oxidative stress, lipid peroxidation, and cell death. Probiotics, conversely, have shown potential in promoting host health and reducing the toxicity of endocrine-disrupting chemicals (EDCs). This study examined whether sub-chronic BPA exposure disrupts hepatic lipid metabolism in female zebrafish (Danio rerio), and whether co-administration of probiotics mitigates these effects. Adult females were exposed for 28 days to the following treatments: 10 µg/L BPA via water (BPA); 10⁹ CFU/g body weight/day of probiotic formulation (P); and both treatments (BPA+P). An untreated group served as a control (CTRL). Hepatic lipid composition was analyzed using UHPLC-QTOF-MS, while liver sections were investigated by Fourier Transform Infrared Imaging (FTIRI) spectroscopy. BPA exposure decreased 14 unsaturated triacylglycerols and lysophosphatidylcholine 18:0, suggesting steatosis onset and inflammation, while in the group exposed to BPA+P, the decrease was limited to 8 triacylglycerols and the reduction in lysophosphatidylcholine 18:0 was prevented. Analyses of pooled liver samples precluded modeling tank-level effects; thus, the results are interpreted as semi-quantitative. Partial least square discriminant analysis built on the comparison of all groups together confirmed an intermediate phenotype for BPA+P fish between BPA and P groups. The observed beneficial role of probiotics in counteracting BPA-related metabolic disturbances was also supported by FTIRI, evidencing the ability to mitigate the effects of BPA on lipid and glycosylated compound metabolism. These findings highlight the potential of probiotic supplementation as a practical and accessible strategy to mitigate BPA-induced metabolic disturbances, contributing to the development of mitigating approaches against environmental contaminant-related liver dysfunction. Full article

Puberty is a neuroendocrine process required for sexual maturity; it is regulated by the hypothalamic–hypophysis–gonadal (HHG) axis. Kisspeptin (KISS1) plays a vital role in activating this axis by stimulating the secretion of gonadotropin-releasing hormone (GnRH). Cadmium (Cd) exposure disrupts KISS1 signaling in female rodents; its effects on hypothalamic gene expression during male puberty remain poorly understood. This study investigated the effects of Cd exposure on hypothalamic Kiss1, Kiss1r, and Gnrh1 expression, preputial separation (PS) as a marker of pubertal onset, testosterone levels, Cd concentration, and total antioxidant capacity (TAC) in the serum and hypothalamus of pubertal male Wistar rats. Animals received once a week intraperitoneal injection of CdCl₂ (1 mg/Kg body weight/100 µL) or saline (100 µL) and were euthanized on postnatal day (PND) 35 or 49. Cd exposure reduced serum testosterone levels and TAC. Also, pubertal onset was delayed. At PND 35, Cd decreased hypothalamic Kiss1 expression, whereas at PND 49, it reduced Kiss1r and Gnrh1 expression. These results suggest that Cd alters hypothalamic gene expression, which may contribute to delayed puberty and impaired sexual maturity. Our findings suggest the vulnerability of puberty to exposure to Cd, acting as an endocrine disruptor and neurotoxicant, with alterations for male reproductive maturity. Full article

Recent scientific evidence confirms that there is no safe threshold for bisphenol A intake, prompting strict regulatory actions and new prohibitions in the European Union. As a result, bisphenol A has increasingly been replaced by other analogues that are also toxic but less regulated and insufficiently studied, posing a new risk to human health due to cumulative exposure. Since food is the primary source of exposure to these compounds, this review aimed to evaluate the most appropriate existing chromatographic methods for their determination under newly introduced near-zero tolerance limits, as well as to assess current cumulative dietary exposure and associated health risks. A systematic literature search was conducted in major scientific databases and relevant regulatory sources covering the period from 2015 to 2025, following PRISMA guidelines. Of the 489 identified publications, 22 met the eligibility criteria for full-text analysis. The findings indicate a clear methodological shift towards simultaneous quantification of multiple bisphenol analogues, with LC-MS/MS emerging as the dominant and most robust analytical technique. Dietary exposure to bisphenol A is expected to decline due to stricter regulations; however, this may trigger a rise in the use of its structural analogues as alternatives. Exposure assessments indicate that combined dietary intake of bisphenol A and its analogues can result in a Hazard Index exceeding 1, primarily due to the substantially reduced Tolerable Daily Intake for bisphenol A. This highlights the need for continuous monitoring under stricter regulatory frameworks. Full article

Disinfection byproducts (DBPs) are ubiquitous contaminants formed during drinking water treatment and are traditionally regulated based on cytotoxic and genotoxic endpoints. However, evidence suggests that DBPs may also act as metabolic disruptors interfering with hepatic metabolic pathways. This study investigates the early metabolic disruption and steatogenic effects of four regulated DBPs, bromoform (BR), bromodichloromethane (BDCM), monochloroacetic acid (MCA), and dichloroacetic acid (DCA), using the human hepatic cell models HepG2 (derived from hepatocellular carcinoma) and HUH7 (derived from hepatoblastoma). Cells were exposed to a broad concentration range (1 pM–100 µM) to capture both sub-cytotoxic and mechanistically informative responses at low, environmentally relevant levels. Effects on lipid and sterol metabolism were assessed through the transcriptional modulation of a panel of nuclear receptors (AHR, PXR, RXR, and LXR) and the sterol regulatory enzyme HMG-CoA reductase (HMGCR) as well as intracellular lipid accumulation; cytotoxicity and oxidative stress endpoints were concurrently evaluated. All DBPs tested induced significant, dose-dependent alterations in nuclear receptor signaling and also promoted lipid accumulation in the low-concentration range and without concurrent cytotoxicity; conversely, oxidative stress responses were limited or absent, and HMGCR emerged as a sensitive target, albeit with different patterns (upregulation by BR and MCA, and downregulation by BDCM and DCA). Relevant substance-specific aspects were also observed for other transcriptional targets, e.g., PXR upregulation was particularly evident for BR and BCDM while DCA downregulated the tested receptors. DBP-induced lipid accumulation was more pronounced in HUH7. Regulated DBPs can elicit early steatogenic and metabolic effects even at concentrations below current regulatory thresholds. The findings highlight that endocrine–metabolic disruption should be considered as a relevant endpoint in DBP risk assessment. Full article

Countless environmental pollutants and xenobiotics, are widespread and linked to hazardous effects, including breast cancer. Due to their lipophilic properties, these accumulate in fat tissue, such as breast adipose tissue. However, little is still known about their combined effects and distribution within the breast microenvironment. Alterations in fatty acid metabolism can be a biomarker for cancer progression and a potential bioindicator of pollutant exposure. In this study, the fatty acid profile and levels of organochlorine and organophosphate pesticides (OCPs and OPPs), polychlorinated biphenyls (PCBs), brominated flame retardants (BFRs), organophosphate esters (OPEs), polycyclic aromatic hydrocarbons (PAHs) and synthetic musks (SMs) were measured in 48 breast adipose tissue samples from breast cancer and healthy patients (controls). Twelve xenobiotics were detected at high frequency rates, and the distribution profile of these pollutants differed between cohorts. In total, 163 correlations were identified between specific fatty acids and breast cancer patients’ data, with distinct correlation patterns between cohorts. Fatty acids show the potential to be biomarkers of the presence of lipophilic xenobiotics in the breast microenvironment; however, more studies are needed. This preliminary study is the first to analyze OPPs, OPEs, and PAHs in breast adipose tissue and report associations between xenobiotics and specific fatty acids. Full article

The ovaries are crucial reproductive organs that regulate the menstrual cycle and support pregnancy through the production of steroid hormones. They are highly susceptible to various environmental pollutants, which can lead to ovarian disorders. Luteal phase defect (LPD) and premature ovarian failure (POF) are common ovarian disorders in women. In this study, we integrate network toxicology with molecular docking and molecular dynamics simulations to elucidate the toxicological mechanisms of Benzo(a)pyrene (BaP), a widespread endocrine disruptor, in LPD and POF. Through systematic data mining of the GeneCards and OMIM databases, we identified 1336 targets associated with LPD and 2066 targets related to POF, as well as 220 BaP targets. Venn diagram analysis revealed 36 potential targets for BaP-induced LPD and 43 for BaP-induced POF. GO and KEGG enrichment analyses suggest that BaP-induced LPD and POF may share toxicological mechanisms. PPI network visualization indicated that EGFR, ESR1, and STAT3 are critical common targets for BaP-induced LPD and POF. Molecular docking and molecular dynamics simulations revealed that BaP exhibits strong binding affinity with all three core genes. In KGN cells modeling LPD and POF phenotypes, cellular experiments confirmed that BaP downregulated EGFR and ESR1 expression while upregulating STAT3 expression, thereby supporting the reliability of these targets in BaP-induced ovarian dysfunction. These findings provide insights into BaP-induced reproductive toxicity and offer a foundation for targeted clinical interventions to mitigate the effects of environmental pollutants on women’s reproductive health. Full article

Background: Di(2-ethylhexyl) phthalate (DEHP) is a high-production-volume plasticizer and ubiquitous environ-mental contaminant with established endocrine-disrupting potential. While zebrafish transcriptomic studies have typically used high concentrations and long exposure windows, less is known about genome-wide responses during late embryogenesis/early larval maturation under environmentally relevant exposures. Here we profiled whole-organism transcriptomic responses to a short DEHP exposure during a developmentally sensitive transition (96–120) hours post-fertilization, hpf) and interpreted responses using differential expression, enrichment analyses, and endocrine-focused protein–protein interaction (PPI) network modeling. Methods: Wild-type AB zebrafish lar-vae (96 hpf) were exposed to DEHP at [10⁻⁹ M] or solvent control for 24 h. Larvae were pooled per replicate (25 lar-vae/pool) and processed for poly(A)-selected RNA-seq. Reads were quality-controlled, aligned to the Danio rerio reference genome, and quantified at gene- level. Differential expression was performed using DESeq2. Functional enrichment used KEGG over-representation analysis (ORA) and gene set enrichment analysis (GSEA). Zebrafish genes were mapped to human orthologs for GO/KEGG and STRING-based endocrine subnetworks, which were visualized and interrogated using STRINGdb and visNetwork. Results: Low-dose, short-term exposure does not produce large gene-level effects but induces coordinated, pathway-level transcriptional remodeling. KEGG ORA showed significant enrichment of MAPK signaling and regulation of actin cytoskeleton with additional enrichment of axon guidance and neuroactive ligand–receptor interaction. GSEA detected coordinated downregulation of KEGG neurodegeneration collections with negative normalized enrichment scores reflecting shared gene sets re-lated to mitochondrial function, proteostasis, cytoskeletal organization, and stress-response pathways. Endo-crine-focused STRING subnetworks indicated consistent downregulation of CYP19A1 within estrogen metabo-lism/biosynthesis modules and downregulation of upstream androgen biosynthetic enzymes HSD3B2 and CYP17A1, alongside upregulation of HSD17B3 and proteostasis-associated factors including DNAJA1. Endocrine network to-pology highlighted regulatory and cofactor nodes affecting receptor-linked transcription, consistent with indirect endocrine modulation rather than large receptor-transcript changes. Conclusions: In summary, this study demon-strates that exposure to low-dose DEHP during a critical period of zebrafish embryonic development is associated with modest but coordinated transcriptomic changes across multiple biological pathways. Pathway enrichment and network-based analyses highlight estrogen- and androgen-associated processes, along with broader signaling, met-abolic, and structural pathways, as transcriptionally responsive during this window. Importantly, these findings reflect molecular-level associations rather than direct evidence of functional or physiological endocrine disruption. Instead, they identify candidate pathways and regulatory networks that may be sensitive to low-level environmen-tal exposure and warrant further investigation. Collectively, this work underscores the value of systems-level tran-scriptomic approaches for detecting subtle, pathway-wide responses to environmentally relevant exposures during development. Full article

Metabolic dysfunction-associated steatotic liver disease (MASLD), formerly known as non-alcoholic fatty liver disease (NAFLD), is becoming the most common liver disease, affecting between 30 and 40% of the global population. MASLD is a multifaceted disease spectrum that is closely associated with obesity, insulin resistance, type 2 diabetes mellitus and, more broadly, metabolic syndrome. All these conditions increase the risk of liver-related mortality, which explains the intense research efforts in recent years to better elucidate its pathogenesis. The crucial impact of environmental pollutants on the development of MASLD is now well recognized. Polychlorinated biphenyls (PCBs) are environmental contaminants that act as endocrine disruptors. Recently, they have been associated with the development of diabetes, obesity, MASLD, and cancer. The association between liver diseases, namely toxicant-associated steatotic liver disease and steatohepatitis (TASLD and TASH, respectively), and occupational exposure to PCBs and other industrial chemicals has been documented by several lines of evidence, whereas the potential role of low-level environmental pollution in liver disease and in MASLD remains incompletely understood. Previous studies on animal models have shown that PCB exposure is associated with steatosis/steatohepatitis, fibrosis, cirrhosis, hepatocellular carcinoma (HCC), altered liver enzymes, and mortality in exposed populations. This review investigates the mechanisms underlying hepatic steatogenesis in preclinical and animal models and analyzes the existing literature on the possible role of PCBs, together with the other conventional risk factors, in the development of MASLD in humans. Full article

Background: Fetal and postnatal development appears to be influenced in multiple ways by exposure to endocrine-disrupting chemicals (EDCs). We used hair biomonitoring to assess the burden of selected EDCs—bisphenol S (BPS), parabens (PBs), triclosan (TCS), and organochlorine pollutants—in pregnant women and their children at birth and at ten months of follow-up. Methods: Hair samples were collected from pregnant women in Crete at delivery and from their infants shortly after birth and during follow-up. The assessment of EDCs’ burden was performed using liquid and gas chromatography–mass spectrometry (LC-MS, GC-MS). Results: Pregnant mothers had higher BPS levels than their infants at birth, whereas at 10 months’ follow-up, infants exhibited markedly higher BPS concentrations than both their birth levels and the maternal levels, indicating increasing postnatal exposure. Infants at birth had higher TCS levels than their mothers; these levels then declined at follow-up. In contrast, mothers contained higher levels of MeP, EthP, BenP, and ButP levels than those of infants, either at birth or at ten months’ follow-up. Organochlorine compounds were present at low but measurable levels. Significant pairwise comparisons were observed for some of the EDC analytes, mostly between mothers and their infants and between mothers and infants at follow-up. Conclusions: These findings demonstrate constant, compound-specific, and time-dependent EDC burdens, highlighting the importance of prenatal EDC exposure in infants at birth and at ten months’ follow-up compared to that of mothers. Full article

Bisphenol A (BPA) is a synthetic organic compound commonly used as a plasticiser in the industry. It pollutes the environment, harms human and animal organisms, and exhibits endocrine-disrupting properties. Companion animals, living in proximity to humans, are highly exposed to BPA. However, knowledge of cat exposure to this compound is extremely scarce. In the present study, BPA levels were analysed for the first time in cat hair using liquid chromatography–triple quadrupole mass spectrometry. BPA concentrations ranged from below the limit of detection to 955.4 pg/mg, with a mean (±standard deviation) of 67.98 ± 145.2 pg/mg and a median of 27.3 pg/mg. Higher levels of BPA have been found in the strictly indoor cats (mean 79.45 ± 162.2 pg/mg, median 35.3 pg/mg) than in cats with outdoor access (mean 25.93 ± 8.07 pg/mg, median 24.4 pg/mg). Some differences in BPA levels have also been noted depending on age and body condition scores. The results show that cats are exposed to BPA to a considerable extent, and the levels of this compound in hair may depend on many factors. It can be assumed that BPA may negatively affect cat health, but due to limited knowledge of BPA metabolism in cats and its harmful effects in this species, many aspects of these issues require further comprehensive studies. Full article