Search Results (217)

Lead (Pb) is a naturally occurring metal that is environmentally ubiquitous due to industrial activities, such as mining, smelting, and fossil fuel combustion. Exposure to Pb adversely affects the central nervous system, gastrointestinal tract, lungs, liver, bones, and cardiovascular system, leading to a multitude of negative health impacts, such as anemia and neurological disorders. While significant research has focused on the effects of Pb on the nervous and immune systems, Pb’s impact as a reproductive endocrine disruptor remains largely understudied. The first objective of this review was to collate the current literature regarding the effects of Pb on the reproductive system of aquatic species (primarily fish) and agricultural livestock to highlight the ecological significance and impacts on animal health. Literature supports the hypothesis that exposure to Pb can impede reproductive processes by affecting hormone levels, reproductive organ development, and fertility. A second objective of this review was to elucidate putative mechanisms underlying Pb as a reproductive endocrine disruptor using molecular data and computational approaches. Based on transcriptomics data, Pb is hypothesized to perturb key pathways important for hypothalamic–pituitary–gonadal axis functions, such as circadian regulation and estrogen receptor signaling. Given the widespread environmental presence of Pb, understanding these mechanisms is essential for improving risk assessments and protecting animal reproductive health. Full article

This study investigates the effects of Bisphenol A (BPA)—a ubiquitous endocrine disruptor—on the swimming behavior of the rotifer Brachionus plicatilis. Across a 0–40 ppm gradient, a biphasic response was observed, with swimming speed peaking at 20 ppm (100.42 ± 12.17 µm/s) and then significantly declining by 43% to 57.58 ± 30.59 µm/s at 40 ppm (Tukey, p < 0.05). Speed–frequency plots revealed co-existing hyper- and hypoactive sub-populations at 10–30 ppm, whereas severe inhibition dominated at 40 ppm. Additionally, temporal analysis confirmed that BPA effects were both concentration- and time-dependent, with the mean speed at 10 ppm declining only slightly over time (slope ≈ −0.8), whereas at 40 ppm, the decrease was an order of magnitude steeper (slope ≈ −16.9). Additionally, BPA exposure also triggered a sharp rise in abrupt turns (582.53 ± 477.55 events) and greater path sinuosity, consistent with neuromuscular disturbance. These findings demonstrate that rotifer locomotion provides an early and sensitive indicator of environmental BPA exposure. Full article

Maternal health has a profound impact on fetal development, influencing the risk of pediatric endocrine disorders both directly and indirectly through various biological and environmental mechanisms. Throughout pregnancy, several endocrine disorders can arise or be exacerbated due to the physiological changes that occur. An in-depth review of articles with evidence-based research discussing the significant effects of maternal endocrinopathies and endocrine disruptors on fetal development and infant health was conducted in this review paper. The most common endocrine disorder during pregnancy is gestational diabetes mellitus, which has an incidence rate of 2–16%, depending on ethnic origin. Maternal diabetes, apart from macrosomia and hypoglycemia, increases the risk for several pregnancy and neonatal complications such as stillbirth, perinatal mortality, and congenital malformations. Other endocrine issues occurring in pregnancy include alterations in thyroid hormone levels, obesity-related insulin resistance, Cushing syndrome, or polycystic ovarian syndrome, which all may negatively influence the fetus, as well as offspring development. Additionally, environmental exposure to harmful substances during pregnancy can disrupt endocrine function. Bisphenol A is the most common endocrine disruptor, which is particularly detrimental during gestation. Bisphenol A exposure is related to low birth weight, preterm birth, or developmental delays. Also, its exposition could be associated with an increased risk of obesity, metabolic disorders, and certain cancers later in life. Endocrinopathies and exposure to endocrine disruptors during pregnancy represent a challenging problem, being widespread and demanding appropriate management to reduce fetal and newborn complications. Full article

Among the numerous compounds released as a result of human activities, endocrine-disrupting chemicals (EDCs) have attracted particular attention due to their widespread detection in human biological samples and their accumulation across various ecosystems. While early research primarily focused on their effects on reproductive health, it is now evident that EDCs may impact neurodevelopment, altering the integrity of neural circuits essential for cognitive abilities, emotional regulation, and social behaviors. These compounds may elicit epigenetic modifications, such as DNA methylation and histone acetylation, that result in altered expression patterns, potentially affecting multiple generations and contribute to long-term behavioral phenotypes. The effects of EDCs may occur though both direct and indirect mechanisms, ultimately converging on neurodevelopmental vulnerability. In particular, the gut–brain axis has emerged as a critical interface targeted by EDCs. This bidirectional communication network integrates the nervous, immune, and endocrine systems. By altering the microbiota composition, modulating immune responses, and triggering epigenetic mechanisms, EDCs can act on multiple and interconnected pathways. In this context, elucidating the impact of EDCs on neurodevelopmental processes is crucial for advancing our understanding of their contribution to neurological and behavioral health risks. Full article

Lindane, a persistent organochlorine pesticide, exerts toxic effects on the female reproductive system, compromising oocyte quality and maturation. However, the effects of this pesticide on mammalian oocyte morphology and ultrastructure remain unknown. This study investigated the effects of Lindane on mouse oocyte ultrastructure using an in vitro model with Transmission Electron Microscopy (TEM) at concentrations from 1 to 100 μM. The results revealed a progressive dose-related trend of alterations: at 1 μM, mild swelling of smooth endoplasmic reticulum (SER) vesicles; at 10 μM, increased SER dilation and cytoplasmic disorganization; and at 100 μM, pronounced vacuolization, mitochondrial swelling, dense lamellar bodies (dlbs), and multivesicular bodies (MVBs) indicative of autophagic activity. Mitochondrial alterations increased significantly with concentration: 3.2 ± 0.8 (control), 5.7 ± 1.0 (1 μM), 9.4 ± 1.5 (10 μM), and 16.8 ± 2.3 (100 μM) altered mitochondria per oocyte (p < 0.01). Vacuole frequency was notably elevated at 100 μM (4.3 ± 1.1 vs. 0.7 ± 0.5 in controls), and mislocalization of organelles within the ooplasm was observed. In conclusion, Lindane-induced oocyte ultrastructural alterations were observed at all tested concentrations but were more pronounced at 100 μM. These results highlight its impact on female fertility and may guide the search for protective agents, as well as efforts to reduce environmental exposure to endocrine disruptors. Full article

A comparative analysis of testicular tumors in dogs and humans highlights notable similarities in cancer behavior, particularly regarding environmental influences. The ubiquitous distribution of endocrine disruptors in industrialized countries and their effects are strongly linked to the development of testicular cancers. This study examined 221 and 174 cases of testicular tumor in dogs and humans, respectively, from the Campania Animal Cancer Registry and the database of the National Cancer Institute “Fondazione G. Pascale-IRCCS”, between 2020 and 2023. These data were integrated with environmental data from the Ministry of Environment and Energy Security website and the Campania Regional Agency for Environmental Protection (ARPAC). The areas with the highest frequency of testicular tumors in both species were the municipalities of Napoli, Salerno, and Caserta, and their corresponding provinces. The same locations experienced severe contamination of soil and water by environmental pollutants, probably correlated to testicular tumors. Although the molecular mechanisms are not yet fully understood, our data suggest a strong link between the frequency of testicular tumors in humans and dogs and high concentrations of environmental pollutants in the reported locations. These findings emphasize the value of dogs as a potential animal model for studying human health and the effect of environmental factors on cancer development. Full article

Background/Objectives: Endocrine disruptors (EDs) are xenobiotic chemicals that disrupt hormone signaling and homeostasis within the human body. Accumulative evidence proposes that EDs could affect systemic hormone balance and local microbial communities, including the female genital tract (FGT) microbiome. The FGT microbiome, and especially the vaginal microbiota, contributes significantly to reproductive health maintenance, defense against infection, and favorable pregnancy outcomes. Disruption of the delicate microbial environment is associated with conditions like bacterial vaginosis, infertility, and preterm birth. Methods: The present narrative review summarizes the existing literature on EDs’ potential for changing the FGT microbiome. We discuss EDs like bisphenol A (BPA), phthalates, and parabens and their potential for disrupting the FGT microbiome through ED-induced hormone perturbations, immune modulation, and epithelial barrier breach, which could lead to microbial dysbiosis. Results: Preliminary evidence suggests that ED exposure–microbial composition changes relationships; however, robust human evidence for EDs’ changes on the FGT microbiome remains scarce. Conclusions: Our review addresses major research gaps and suggests future directions for investigation, such as the necessity for longitudinal and mechanistic studies that combine microbiome, exposome, and endocrine parameters. The relationship between EDs and the FGT microbiome could be critical for enhancing women’s reproductive health and for steering regulatory policies on exposure to environmental chemicals. Full article

Plastic manufacturing involves using compounds that could be considered endocrine disruptors. Consequently, concern about the effect of these particles on the hormonal regulation of various systems, including the hypothalamic–pituitary–thyroid axis, has been increasing. By applying the Amphibian Metamorphosis Assay (AMA), the effects of irregular polystyrene microplastics (PS) MPs on the thyroid gland of Xenopus laevis were investigated. The histological effects on other organs of tadpoles were also studied. Tadpoles were exposed to 500 and 50 µg of virgin PS MP particles, (200 µm range)/L, administered by diet for 21 days. PS dietary exposure revealed statistically significant effects for the snout to vent length and the whole body length apical endpoints on day 21. The histological survey of both treatment groups revealed no noteworthy effects on the thyroid gland, digestive tract, or kidneys, but slight modifications to the liver. Mild ultrastructural modifications were detected in tadpoles’ enterocytes and hepatocytes in both treatment groups, but were likely to be reversible. Overall, our results contrast with previous research results in which effects were observed, but using different types, concentrations, and numbers of MPs. All this suggests the need for standardized methods for the environmental risk assessment of MPs/NPs (nanoplastics). Concern about the risk of NPs seems to be greater, and more studies with NP particles should be conducted. Full article

The increasing presence of emerging contaminants in aquatic environments, particularly endocrine disruptors (EDs), has raised significant environmental and public health concerns due to their toxicity, persistence, and ability to interfere with the endocrine systems of both aquatic organisms and humans. Among these compounds, the steroid hormones 17β-estradiol (E2) and 17α-ethinylestradiol (EE2) stand out, as they are frequently detected in wastewater, even after conventional treatment processes, which often exhibit limited removal efficiency. In this context, advanced oxidation processes (AOPs), especially those based on the generation of sulfate radicals (SO₄•⁻), have emerged as promising alternatives due to their high redox potential, extended half-life, and broad effectiveness across various pH levels. This work reviews recent advances in AOPs for the degradation of E2 and EE2, focusing on sulfate radical-based processes. The main degradation mechanisms, operational parameters, removal efficiency, challenges for large-scale application, and gaps in the current literature are discussed. The analysis indicates that despite their high effectiveness, sulfate radical-based processes still require further investigation in real wastewater matrices, the assessment of the toxicity of by-products, and the optimization of operational variables to be established as viable and sustainable technologies for wastewater treatment. Full article

Background/Objectives: In 4-octylphenol (4-OP), a toxic environmental pollutant with endocrine disruptive effect, the use of 4-OP causes pollution in the freshwater environment and poses risks to aquatic organisms. Common carps (Cyprinus carpio L.) live in freshwater and are experimental animals for studying the toxic effects of environmental pollutants on fish. Its heart is susceptible to toxicants. However, whether 4-OP has a toxic effect on common carp heart remains unknown. Methods: Here, we conducted a common carp 4-OP exposure experiment (carp treated with 17 μg/L 4-OP for 45 days), aiming to investigate whether 4-OP has a toxic effect on common carp hearts. We observed the microstructure and ultrastructure of carp heart and detected autophagy genes, mitochondrial fission genes, mitochondrial fusion genes, glycolytic enzymes, AMPK, ATPase, and oxidative stress factors, to investigate the molecular mechanism of 4-OP induced damage in common carp hearts. Results: Our results showed that 4-OP exposure caused mitochondrial damage, autophagy, and damage in common carp hearts. 4-OP exposure increased the levels of miR-144, and eight autophagy factors (Beclin1, RB1CC1, ULK1, LC3-I, LC3-II, ATG5, ATG12, and ATG13), and decreased the levels of four autophagy factors (PI3K, AKT, mTOR, and SQSTM1). Furthermore, 4-OP exposure induced the imbalance between mitochondrial fission and fusion and mitochondrial dynamics imbalance, as demonstrated by the increase in three mitochondrial fission factors (Mff, Drp1, and Fis1) and the decrease in three mitochondrial fusion factors (Mfn1, Mfn2, and Opa1). Moreover, excess 4-OP treatment caused energy metabolism disorder, as demonstrated by the reduction in four ATPase (Na⁺K⁺-ATPase, Ca²⁺Mg²⁺-ATPase, Ca²⁺-ATPase, and Mg²⁺-ATPase), elevation in four glycolysis genes (HK1, HK2, LDHA, and PGK1), reduction in glycolysis gen (PGAM2), and the elevation in energy-sensing AMPK. Finally, 4-OP treatment induced the imbalance between antioxidant and oxidant and oxidative stress, as demonstrated by the increase in oxidant H₂O₂, and the decreases in five antioxidant factors (CAT, SOD, T-AOC, Nrf2, and HO-1). Conclusions: miR-144 mediated autophagy by targeting PI3K, mTOR, and SQSTM1, and the miR-144/PI3K-AKT-mTOR/ULK1 pathway was involved in 4-OP-induced autophagy. Mff-Drp1 axis took part in 4-OP-caused mitochondrial dynamics imbalance, and mitochondrial dynamics imbalance mediated autophagy via Mfn2-SQSTM1, Mfn2/Beclin1, and Mff-LC3-II axes. Energy metabolism disorder mediated mitochondrial dynamics imbalance through the AMPK-Mff-Drp1 pathway. Oxidative stress mediated energy metabolism disorder via the H₂O₂-AMPK axis. Taken together, oxidative stress triggered energy metabolism disorder, induced mitochondrial dynamics imbalance, and caused autophagy via the H₂O₂-AMPK-Mff-LC3-II pathway. Our study provided references for the toxic effects of endocrine disruptor on common carp hearts, and provided a basis for assessing environmental pollutant-induced damage in common carp heart. We only studied the toxic effects of 4-OP on common carp, and the toxic effects of 4-OP on other fish species need to be further studied. Full article

Bisphenol A (BPA) is a widespread environmental endocrine disruptor with significant neurodevelopmental and behavioral risks. The present study explored the role of the circadian clock protein NR1D1 in mediating BPA-induced anxiety-like behavior and brain inflammation early in life. Zebrafish embryos exposed to BPA exhibited anxiety-like behavior characterized by altered motor activity patterns. Notably, BPA exposure suppressed the expression of the circadian clock gene nr1d1, accompanied by increased transcriptional and protein levels of pro-inflammatory cytokines, including IL-6, IL-1β, and TNF-α. These changes created a pro-inflammatory microenvironment that disrupted dopamine system homeostasis, contributing to the observed behavioral abnormalities. Activation of NR1D1 using GSK effectively reversed BPA-induced inflammatory responses and restored normal dopamine levels and behavioral phenotypes. These findings highlight NR1D1 as a critical regulator linking circadian rhythm disruption, neuroinflammation, and dopaminergic dysfunction to anxiety-like behavior. This study provides novel insights into the mechanisms underlying BPA-induced neurotoxicity and identifies NR1D1 as a potential therapeutic target for mitigating the adverse effects of early-life BPA exposure. Full article

Ageing is influenced by a complex interplay of genetic, environmental, and lifestyle factors, with increasing evidence highlighting the exposome as a key determinant of healthspan. This review explores the impact of environmental exposures, focusing in particular on pollution, endocrine disruptors, and climate change on the development of age-related diseases such as cardiovascular diseases (CVDs), cancer, and metabolic disorders. Additionally, it examines protective factors that contribute to healthy ageing. A comprehensive literature review was conducted using PubMed, Scopus, and Google Scholar, focusing on studies published between 2000 and 2025. Findings indicate that chronic exposure to pollutants accelerates cellular ageing through mechanisms such as oxidative stress, inflammation, and epigenetic dysregulation. In contrast, longevity hotspots—Blue Zones, Cilento and the mountain villages of Sicily (Sicani and Madonie Mountains)—illustrate how traditional dietary patterns, strong social structures, and reduced environmental toxicity contribute to exceptional health and longevity. Mechanistically, exposome-driven alterations in immune-inflammatory pathways and epigenetic regulation play a central role in modulating ageing trajectories. Understanding these interactions is essential for developing targeted strategies to mitigate harmful exposures and enhance protective factors. This review underscores the urgent need for integrative public health policies that address the environmental determinants of ageing, ultimately promoting a longer and healthier lifespan. Full article

Phthalates are compounds widely used as very effective plasticizers of PVC. Unfortunately, they are also widely known to be endocrine disruptors and are detrimental to human health and the environment. For this reason, environmentally friendly plasticizers are being intensively sought after in response to the market needs in the context of sustainable development and legislative changes regarding the use of phthalates. Our research presents an innovative approach to addressing this problem. In this paper, we propose new biobased oligoesters as non-toxic and harmless plasticizers of poly(vinyl chloride). New plasticizers were obtained by polyesterification of saturated dimerized fatty acid (DFA), adipic acid (ADA), triethylene glycol (TEG), and 2-ethylhexanol (2-EH), and were characterized by nuclear magnetic resonance, size exclusion chromatography, and viscosity analyses. The compatibility of the obtained oligoesters with PVC was determined using the method for obtaining PVC films by casting from a THF solution. Selected plasticizers were used to obtain PVC blends at 50 phr. They were then tested for plasticizer migration, hardness, thermogravimetric analysis, differential scanning calorimetry, and mechanical strength. Their properties were compared with the commercially available monomeric plasticizers di(2-ethylhexyl) terephthalate and di(2-ethylhexyl) adipate. The conducted study shows that the oligoesters obtained at a molar ratio of ADA to DFA of 9:1 and using an excess of 2-EH exhibit very good compatibility and plasticizing ability. The use of higher amounts of DFA worsens the compatibility of the oligoesters with PVC. However, a 4:1 ADA-to-DFA molar ratio produced results that still allow for the use of these compounds as plasticizers at lower concentrations or in combination with other plasticizers. Full article

This study successfully developed a novel molecularly imprinted ultrafiltration membrane (MIUM) for energy-efficient and selective removal of dibutyl phthalate (DBP) from wastewater. Guided by Gaussian simulations, methacrylic acid (MAA) was identified as the optimal functional monomer, achieving the strongest binding energy (ΔE = −0.0698 a.u.) with DBP at a 1:6 molar ratio, providing a foundation for precise cavity construction. DBP-imprinted polymers (MIPs) synthesized via bulk polymerization were integrated into polysulfone membranes through phase inversion. The optimized MIUM (81.27% polymer content) exhibited exceptional performance under low-pressure operation (0.2 MPa), with a water flux of 111.49 L·m²·h⁻¹ and 92.87% DBP rejection, representing a 43% energy saving compared to conventional nanofiber membranes requiring 0.4 MPa. Structural characterization confirmed synergistic effects between imprinted cavities and membrane transport properties as the key mechanism for efficient separation. Notably, MIUM demonstrated remarkable selectivity, achieving 91.57% retention for DBP while showing limited affinity for structurally analogous phthalates (e.g., diethyl/diisononyl phthalates). The membrane maintained > 70% retention after 10 elution cycles, highlighting robust reusability. These findings establish a paradigm for molecular simulation-guided design of selective membranes, offering an innovative solution for low-energy removal of endocrine disruptors. The work advances wastewater treatment technologies by balancing high permeability, targeted pollutant removal, and operational sustainability, with direct implications for mitigating environmental risks and improving water quality management. Full article

Bisphenol A (BPA) is a common synthetic chemical compound classified as an endocrine disruptor. It affects multiple physiological systems in the body, including the female reproductive system, particularly granulosa cells (GCs) in the ovaries, where steroidogenesis occurs. This study investigated the impact of various BPA concentrations (environmentally relevant concentrations of 0.001 µM and 0.1 µM and toxicological concentration of 100 µM) and exposure times (24 and 72 h) on cell viability and counts and in vitro production of estradiol and progesterone in human GCs collected from waste follicular fluid of IVF patients. Gene expression analysis of 182 genes associated with steroidogenesis and apoptosis was performed in GCs using PCR arrays, followed by protein expression analysis by Western blot. Our results demonstrate that after longer BPA exposure (72 h), a higher concentration of BPA (100 µM) negatively affects the cellular viability and counts and significantly alters steroid hormone biosynthesis in vitro, leading to reduced concentrations of estradiol and progesterone in the culture medium. We found that all BPA concentrations altered the expression of different steroidogenesis- and apoptosis-related genes in GCs. At 0.001 μM, BPA exposure decreased the expression of TRIM25, UGT2B15, CASP3, and RPS6KA3 genes and increased the expression of NR6A1 and PPID genes. At 0.1 μM, BPA increased the expression of AR, HSD3B1, BID, IKBKG, and PPID genes while reducing the expression of TRIM25 and CASP3 genes. At the highest concentration of 100 μM, BPA upregulated the expression of AR, GPER30, BID, IKBKG, and PPID genes and downregulated the expression of FOXO1 and UGT2B15 genes. These results highlight BPA’s concentration-specific effects on steroidogenesis and apoptosis and show its potential to compromise GC function, with possible negative implications for female fertility and ovarian health, even at environmentally relevant concentrations. Full article