Search Results (1,311)

Endocrine disruptors contaminate indoor and outdoor air, water, and food. Besides modifications of the androgen/estrogen balance, endocrine disruptors can alter thyroid function, metabolic balance, immune defenses, and brain development during fetal life, childhood, and adolescence. Among the consequences of fetal exposure to endocrine disruptors, neurobehavioral disorders, particularly psychiatric disorders (for example, schizophrenia and bipolar disorder), attention deficit disorders, and mood disorders, occupy a special place. Therefore, endocrine disruptors are also neuroendocrine disruptors. This review article first summarizes the direct and transgenerational effects of endocrine disruptors. Then, data from a French national cohort of patients whose mothers were treated with synthetic hormones (estrogens and/or progestogens) during their pregnancy(ies) are used to describe the psychiatric disorders developed by children exposed in utero and the multigenerational and potentially transgenerational impacts. Full article

Bisphenol A (BPA) and its substitutes have been identified as endocrine-disrupting chemicals (EDCs). However, little information is available on their reproductive endocrine disruptive effects in mollusks. This study cloned the full-length sequence (2434 bp) of the estrogen-related receptor (ERR) gene in the freshwater bivalve Corbicula fluminea and performed a bioinformatics analysis and tissue-specific expression analysis. We further examined the expression of the CfERR gene after exposure to E2, BPA, and their substitutes (BPS, BPF, and BPAF) at 1, 10, and 100 μg/L for 0, 1, 7, 14, 21, and 28 days. The results showed that CfERR is a nuclear protein with a typical structure. Phylogenetic analysis indicated a high degree of similarity among bivalve species. The high expression of CfERR in the gonad suggested its important role in reproductive regulation. The exposure experiment confirmed that CfERR showed a time- and dose-dependent upregulation in response to all pollutants, with BPS and BPAF exhibiting stronger estrogenic interference effects. This study facilitates a better understanding of the reproductive regulation of bivalves and provides data to support the toxicity evaluation of BPA and its substitutes. Full article

Many common chemicals are known or suspected to harm brain development, and children are particularly vulnerable, yet research on their long-term effects on mental health is limited. This study investigated the associations of early childhood exposure to endocrine disrupting and neurotoxic chemicals with the development of internalizing, externalizing, and attention-deficit/hyperactivity disorder (ADHD) symptoms from early childhood through adolescence in 387 children from the Rhea cohort in Crete, Greece. At age 4, serum concentrations of 3 organochlorine pesticides and 14 polychlorinated biphenyls, and urinary concentrations of 7 phthalate metabolites and 6 dialkyl phosphate metabolites were measured. Children’s symptoms were assessed via maternal reports at ages 4, 6, 11 and 15 years. Using generalized estimating equation models, the study found that early exposure to hexachlorobenzene (HCB) and dichlorodiphenyldichloroethylene (DDE) was associated with increased externalizing symptoms across ages in girls [beta (95% CI): 0.20 (0.04, 0.37) and 0.11 (0.01, 0.21), respectively]. Among girls, low molecular weight (LMW) phthalates were also linked to elevated internalizing and externalizing symptoms, as well as ADHD-related difficulties [beta (95% CI): 0.15 (0.04, 0.26), 0.13 (0.01, 0.25), and 0.13 (0.02, 0.24), respectively]. Additionally, exposure to organophosphate pesticides was associated with increased externalizing and ADHD symptoms [beta (95% CI): 0.13 (0.04, 0.22) and 0.12 (0.04, 0.20), respectively]. The findings suggest that early childhood exposure to environmental chemicals may have long-term effects on emotional and behavioral development, with pronounced effects observed only in girls. Full article

Fluoride is a widespread environmental toxin that disrupts metabolic and endocrine functions, but its impact on pancreatic inflammation and hormone secretion remains unclear. This study examined how chronic fluoride exposure affects pancreatic inflammation and secretory function in rats. Pregnant Wistar rats received sodium fluoride (NaF) at 50 mg/L in drinking water during gestation and lactation. Male offspring continued exposure until 3 months old. Controls received fluoride-free water. Pancreatic tissue and serum were collected. Fluoride levels were measured potentiometrically. Eicosanoids were quantified by SPE and HPLC. Serum insulin, glucagon, and somatostatin were measured by ELISA. Histological and biochemical markers of inflammation and oxidative stress were assessed. Fluoride exposure did not lead to significant accumulation in the pancreas or serum. However, fluoride-exposed rats exhibited a significant decrease in serum insulin and somatostatin concentrations, while glucagon levels remained unchanged. Additionally, the pancreas of fluoride-treated animals showed markedly elevated levels of pro-inflammatory eicosanoids, including prostaglandin E2, leukotrienes A4 and B4, and HETE/HODE derivatives, indicating activation of cyclooxygenase and lipoxygenase pathways. Sustained low-dose fluoride exposure induced pancreatic inflammation and disrupted endocrine homeostasis in rats. These findings suggest that chronic fluoride intake may impair insulin secretion and promote pre-diabetic alterations, warranting further research. Full article

Consumption of meat singed with non-standard fuels is a common practice in many low- and middle-income settings, yet it may introduce combustion-derived toxicants with serious health consequences. While the toxicological effects of pollutants such as polycyclic aromatic hydrocarbons and heavy metals are well documented, the specific impact of singed meat consumption on endocrine regulation remains poorly understood. Of particular concern is the reproductive hormonal network, which not only serves as a sensitive biomarker of systemic disruption but also represents an evolutionary safeguard of fertility and generational continuity. Our study addresses this knowledge gap using male Wistar rats fed for 90 days (week 0 to week 12) on diets containing increasing proportions (25%, 50%, 75%) of meat singed with firewood, liquefied petroleum gas (LPG), or tyres. Firewood- and tyre-singed meat induced dose- and source-dependent toxicity, including hepatocellular injury, impaired protein metabolism, elevated blood urea nitrogen and creatinine, organ hypertrophy, and pronounced oxidative stress. Hormonal analysis revealed reduced testosterone alongside increased FSH, LH, and prolactin, indicating hypothalamic–pituitary–gonadal axis disruption and reproductive risk. In contrast, LPG-singed meat caused only minor alterations. These findings highlight reproductive hormones as sensitive biomarkers, underscoring the health risks of singeing practices and their evolutionary implications for fertility and population fitness. Full article

Mast cells (MCs) belong to the cell network that regulates uterine spiral artery remodeling (uSAR), a critical vascular adaptation supporting placental development and fetal growth. Our previous in vitro study demonstrated that human MCs promote trophoblast invasion, as well as uterine vascular smooth muscle cells (uVSMCs) migration and transition to a synthetic phenotype—essential steps for a successful uSAR. Although MCs are known targets of bisphenol A (BPA), a widespread endocrine-disrupting chemical, its impact on their supportive role in uSAR is unknown. In this study, we used murine cell lines to investigate whether BPA (0.1–100 µM) affects MC-mediated promotion of cellular processes critical for uSAR. Our results showed that BPA exposure hindered MCs’ ability to promote trophoblast invasion and the switch in uVSMCs’ synthetic phenotype and migration. The highest concentrations of BPA altered the expression of genes related to MCs activation and proliferation, and of those involved in trophoblasts invasion. In contrast, low doses induced the expression of pro-inflammatory mediators in MCs without detectable effect on trophoblasts at the transcriptional level. These findings confirmed MCs as key mediators of uSAR, and identified BPA as a disruptor of their function, emphasizing its potential harmful impact on reproductive health. Full article

Bisphenol A (2,2-bis(4-hydroxyphenyl)propane, BPA), an endocrine-disrupting chemical with recognized adverse effects on human health and ecosystems, urgently requires convenient, sensitive, and accurate detection methods. In this study, a hierarchical heterostructure was fabricated by incorporating Ti₃C₂T_x MXene and mesoporous hollow carbon spheres (MHCs) to develop a high-performance electrochemical sensor for BPA. The nanocomposite was thoroughly characterized using SEM, TEM, and XRD, and then applied to modify a glassy carbon electrode (GCE). Under optimized conditions including pH and accumulation time, BPA detection was carried out via differential pulse voltammetry (DPV). The sensor exhibited a wide linear detection range from 10 to 200 μM and a low detection limit of 2.6 μM. Moreover, it was successfully applied to environmental water samples, demonstrating high accuracy and practicality for real-world BPA monitoring. Full article

Chronic kidney disease (CKD) affects nearly 10% of the global population, ranks among the top ten causes of death, and often progresses silently to end-stage disease without timely intervention. Increasing evidence indicates that many adult-onset cases originate in early life through adverse influences on kidney development, a process termed kidney programming within the Developmental Origins of Health and Disease (DOHaD) framework. Environmental pollutants are now recognized as key drivers of kidney injury across the life course. Heavy metals, air pollutants, plastic contaminants such as bisphenol A, phthalates, and micro/nanoplastics—as well as biocontaminants like mycotoxins and aristolochic acid—and chronic light pollution can accumulate in kidney tissue or act systemically to impair function. These exposures promote oxidative stress, inflammation, and endothelial and circadian disruption, culminating in tubular injury, glomerular damage, and fibrosis. Notably, early-life exposures can induce epigenetic modifications that program lifelong susceptibility to CKD and related complications. Oxidative stress is central to these effects, mediating DNA, lipid, and protein damage while influencing developmental reprogramming during gestation. Preclinical studies demonstrate that antioxidant-based interventions may mitigate these processes, providing both renoprotective and reprogramming benefits. This review explores the mechanistic links between environmental pollutants, oxidative stress, and kidney disease and highlights antioxidant strategies as promising avenues for prevention and intervention in vulnerable populations. Full article

Per- and polyfluoroalkyl substances (PFAS) are a diverse group of synthetic fluorinated compounds widely used in industrial and consumer products due to their exceptional thermal stability and hydrophobicity. However, these same properties contribute to their environmental persistence, bioaccumulation, and potential adverse health effects, including hepatotoxicity, immunotoxicity, endocrine disruption, and increased cancer risk. Traditional water treatment technologies, such as coagulation, sedimentation, biological degradation, and even advanced membrane processes, have demonstrated limited efficacy in removing PFAS, as they primarily separate or concentrate these compounds rather than degrade them. In response to these limitations, photoassisted processes have emerged as promising alternatives capable of degrading PFAS into less harmful products. These strategies include direct photolysis using UV or VUV irradiation, heterogeneous photocatalysis with materials such as TiO₂ and novel semiconductors, light-activated persulfate oxidation generating sulfate radicals, and photo-Fenton reactions producing highly reactive hydroxyl radicals. Such approaches leverage the generation of reactive species under irradiation to cleave the strong carbon–fluorine bonds characteristic of PFAS. This review provides a comprehensive overview of emerging photoassisted technologies for PFAS removal from water, detailing their fundamental principles, degradation pathways, recent advancements in material development, and integration with hybrid treatment processes. Moreover, it discusses current challenges related to energy efficiency, catalyst deactivation, incomplete mineralization, and scalability, outlining future perspectives for their practical application in sustainable water treatment systems to mitigate PFAS pollution effectively. Full article

Bisphenol A (BPA) is classified as an endocrine disruptor that mainly mimics the effects of estrogen and disrupts the synthesis of male androgens. Due to the toxicity of BPA, some new analogs, such as bisphenol BPB, BPC, BPF, PBH, and BPZ, were introduced into the market. The goal of this research was to demonstrate the applicability of kinetic analysis, in particular, Lineweaver-Burk plots, in assessing the impact of bisphenol Z on enzymatic activity. This study aimed to characterize the inhibitory effects of BPZ on 11β-hydroxysteroid dehydrogenase 1 (11β-HSD1) activity in the transformation of 11-dehydrocorticosterone (DHC) to corticosterone (CORT). During the determination of the enzymatic reaction product, chromatographic analysis conditions were optimized using gradient elution and an Acquity UPLC BEH C18 chromatographic column. The retention time of the assayed corticosterone was approximately 2 min. Also described and compared were graphical methods of analysis and data interpretation, such as Lineweaver-Burk, Eadie-Hofstee, and Hanes-Woolf plots. The experiments demonstrated that bisphenol Z is a mixed 11β-hydroxysteroid dehydrogenase 1 (11β-HSD1) inhibitor, responsible for catalyzing the conversion of 11-dehydrocorticosterone (DHC) to corticosterone (CORT). This relationship was confirmed by analyzing Lineweaver-Burk plots, which showed an increase in apparent K_M with a decrease in the constant V_max, suggesting a mixed inhibition mechanism. Molecular docking and detailed analysis of the interaction profiles revealed that BPZ consistently occupies the active site cavities of all examined enzymes (rat and human 11β-HSD1 and Arabidopsis 11β-HSD2), forming a stabilizing network of non-covalent interactions. Our research has significant biological significance considering the role of the 11β-HSD1 enzyme in the conversion of DHC to CORT and the importance of this process and its functions in adipose tissue, the liver, and the brain. Full article

Background/Objectives: Thyroid dysfunction (hypo- and hyperthyroidism) and cancer incidence have increased over the past decades, possibly linked to environmental contributions from endocrine disrupting chemicals (EDCs). Glyphosate is one of the most widely used herbicides globally and has endocrine-disruptive properties. Because of the sensitivity of the thyroid gland to endocrine disruption and the increased glyphosate exposure worldwide, this comprehensive review aimed to summarize studies investigating the link between glyphosate/glyphosate-based herbicides (GBHs) and thyroid dysfunction in human, animal, and in vitro studies. Methods: PubMed, Scopus, and Embase were used to search for original studies assessing glyphosate or GBH exposure and thyroid-related outcomes through December 2024. Data were extracted on study design, population or model, exposure, and thyroid outcomes. A total of 28 studies, including 9 human, 3 in vitro, and 16 animal studies were included. Results: Human studies showed mixed findings with some suggesting associations between glyphosate exposure and altered thyroid hormone levels, while others found no significant effects. Animal studies, particularly in rodents and amphibians, showed thyroid hormone disruption and altered gene expression, especially after perinatal or developmental exposure. In vitro studies reported changes in thyroid-related gene transcription and cell viability, however at concentrations exceeding those seen in humans. Conclusions: While there is some evidence that glyphosate may disrupt thyroid function, differences in study populations, exposure assessment methods, species models, and exposure doses complicated the comparison and summarization of the results. Further mechanistic and longitudinal studies are needed to clarify the thyroid-specific risks of glyphosate exposure. Full article

Per- and polyfluoroalkyl substances (PFASs) are highly chemically stable synthetic compounds. They are widely used in industrial and commercial sectors due to their ability to repel water and oil, thermal stability, and surfactant properties. However, this stability results in environmental persistence and bioaccumulation, posing significant health risks as PFASs eventually find their way into environmental media. Key PFAS compounds, including PerFluoroOctanoic Acid (PFOA), PerFluoroOctane Sulfonic acid (PFOS), and PerFluoroHexane Sulfonic acid (PFHxS), have been linked to hepatotoxicity, immunotoxicity, neurotoxicity, and endocrine disruption. In response to the health threats these substances pose, global regulatory measures, such as the Stockholm Convention restrictions and national drinking water standards, have been implemented to reduce PFAS exposure. Despite these efforts, a lack of universally accepted definitions or comprehensive inventories of PFAS compounds hampers the effective management of these substances. As definitions differ across regulatory bodies, research and policy integration have become complicated. PFASs are broadly categorized as either perfluoroalkyl acids (PFAAs), precursors, or other fluorinated substances; however, PFASs encompass over 5000 distinct compounds, many of which are poorly characterized. PFAS contamination arises from direct industrial emissions and indirect environmental formation, these substances have been detected in water, soil, and even air samples from all over the globe, including from remote regions like Antarctica. Analytical methods, such as primarily liquid and gas chromatography coupled with tandem mass spectrometry, have advanced PFAS detection. However, standardized monitoring protocols remain inadequate. Future management requires unified definitions, expanded monitoring efforts, and standardized methodologies to address the persistent environmental and health impacts of PFAS. This review underscores the need for improved regulatory frameworks and further research. Full article

Nonylphenol ethoxylates (NPEOs) are widely utilized in pesticide formulations and industrial products but are known for their endocrine-disrupting properties. Consequently, substitutes such as tristyrylphenol ethoxylates (TSPEOs) have been introduced as inert ingredients in pesticide formulations. Here, we showed that TSPEOs exhibited subacute toxicity in male mice. For the first time, we studied the differences in subacute toxicity (28-day exposure) and the potential toxic effects of TSPEOs with varying polymerization degrees, specifically agricultural emulsifier (AE) #602 and AE #604, in male mice. We demonstrate that AE #602 can induce liver injury, as evidenced by hepatocyte swelling and vacuolar degeneration across all treated groups, along with significant hepatocellular necrosis in the high-dose group. These pathological changes were associated with alterations in oxidative stress biomarkers, including a significant decrease in malondialdehyde levels (0.57 times in the high-dose group, p < 0.05) and increased activities of glutathione peroxidase (up to 1.27 times, p < 0.05) and glutathione, suggesting a potential adaptive compensatory response. Both TSPEOs were found to cause gastric injury according to the results of organ indices and histopathological analyses. AE #604, with lower polymerization degree, caused more severe gastric injury than AE #602. Our findings indicate that NPEO substitutes should be tested for hepatotoxicity and gastrotoxicity and highlight the need for further research into the toxicity differences induced by varying degrees of polymerization of TSPEOs on human health. Full article

This study aims to elucidate the neurodevelopmental toxicity and molecular mechanisms of endocrine-disrupting chemicals (EDCs) in neurodevelopmental disorders (NDDs) through a network toxicology approach, using triclosan exposure as a case example. Potential targets of triclosan were identified via comparative analysis of toxicogenomics databases such as the Comparative Toxicogenomics Database (CTD), Similarity Ensemble Approach (SEA), SwissTargetPrediction, and TargetNet. NDD-related targets were retrieved from GeneCards, Disease Gene Network (DisGeNET), and Online Mendelian Inheritance in Man (OMIM), resulting in 633 overlapping genes associated with disease pathology and triclosan effectors. Protein–protein interaction networks were constructed using STRING and Cytoscape, applying median-based algorithms to identify six core genes: AKT1, TP53, EGFR, FN1, SRC, and ESR1. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses via Metascape revealed that triclosan-induced NDDs are primarily associated with endocrine signaling disruption and activation of the PI3K-Akt pathway. Molecular docking with CB-Dock2 demonstrated strong binding affinities between triclosan and the core targets, while YASARA molecular dynamics simulations confirmed stable interactions, notably with EGFR, exhibiting high binding stability. Collectively, these findings delineate the potential molecular mechanisms underlying triclosan-induced NDDs and underscore the utility of network toxicology, molecular docking, and molecular dynamics simulations in assessing neurotoxicity and related molecular pathways. This research provides novel insights for future investigations, enhances understanding of the potential impact of neurodevelopmental disorders on health, and lays a scientific foundation for the development of preventive and therapeutic strategies. Full article

Nanoplastics have emerged as significant global pollutants, drawing worldwide concern. Due to their small particle size, large specific surface area, and high surface activity, nanoplastics can combine with other environmental contaminants, including environmental nanoparticles, persistent organic pollutants, antibiotics, and endocrine-disrupting chemicals. This review summarizes recent progress on the environmental behavior of nanoplastics and their complex effects on food safety when co-exposed to various contaminants. These composite pollutants accumulate in foods and the environment, and are ultimately taken up by humans, posing potential toxic effects on human health. In the future, the interaction mechanisms between environmental NPs and various co-contaminants, as well as their transfer routes from food to humans, should be addressed. Full article