Search Results (1,156)

Globally, endometriosis affects almost 10% of reproductive-aged women, leading to chronic pain and discomfort. Endocrine-disrupting compounds (EDCs) seem to play a pivotal role as a causal factor. The current manuscript aims to explain potential molecular pathways, synthesize current evidence regarding EDCs as causative agents of endometriosis, and highlight implications in the general population and clinical work. A thorough review of experimental, epidemiologic, and mechanistic research studies was conducted to explain the association between EDCs and endometriosis. Among the primary EDCs under investigation are polychlorinated biphenyls, dioxins, phthalates, and bisphenol A (BPA). Despite methodological heterogeneity and some discrepancies, epidemiologic evidence supports a positive association between some increased levels of BPA, phthalates, and dioxins in urine or in blood, and endometriosis. Experiments support some effect of EDCs on endometrial cells and causing endometriosis. EDCs function as xenoestrogens, alter immune function, induce oxidative stress, and disrupt progesterone signaling. Epigenetic reprogramming may play a role in mediating EDC-induced endometriosis. Endocrine, immunological, and epigenetic pathways link EDCs and endometriosis. Prevention techniques require deeper comprehension of those factors. Causal linkages and possible treatment targets should be based on longitudinal studies and multi-omics techniques. Restriction of EDCs could be beneficial for endometriosis prevalence limitation. Full article

Bisphenol A (BPA), a prevalent endocrine-disrupting chemical, is widely found in various consumer products and poses significant health risks, particularly through hormone receptor interactions, oxidative stress, and mitochondrial dysfunction. BPA exposure is associated with reproductive, metabolic, and neurodevelopmental disorders. Melatonin, a neurohormone with strong antioxidant and anti-inflammatory properties, has emerged as a potential therapeutic agent to counteract the toxic effects of BPA. This review consolidates recent findings from in vitro and animal/preclinical studies, highlighting melatonin’s protective mechanisms against BPA-induced toxicity. These include its capacity to reduce oxidative stress, restore mitochondrial function, modulate inflammatory responses, and protect against DNA damage. In animal models, melatonin also mitigates reproductive toxicity, enhances fertility parameters, and reduces histopathological damage. Melatonin’s ability to regulate endoplasmic reticulum (ER) stress and cell death pathways underscores its multifaceted protective role. Despite promising preclinical results, human clinical trials are needed to validate these findings and establish optimal dosages, treatment durations, and safety profiles. This review discusses the wide range of potential uses of melatonin for treating BPA toxicity and suggests directions for future research. Full article

As typical environmental hormones, endocrine-disrupting chemicals (EDCs) have become a global environmental health issue of high concern due to their property of interfering with the endocrine systems of organisms. As a commonly used substitute for bisphenol A (BPA), bisphenol E (BPE) has been frequently detected in environmental matrices such as soil and water in recent years. Existing research has unveiled the developmental and reproductive toxicity of BPE; however, only one in vitro cellular experiment has preliminarily indicated potential neurotoxic risks, with its underlying mechanisms remaining largely unelucidated in the current literature. Potential toxic mechanisms and action targets of BPE were predicted using the zebrafish model via network toxicology and molecular docking, with RT-qPCRs being simultaneously applied to uncover neurotoxic effects and associated mechanisms of BPE. A significant decrease (p < 0.05) in the frequency of embryonic spontaneous movements was observed in zebrafish at exposure concentrations ≥ 0.01 mg/L. At 72 hpf and 144 hpf, the larval body length began to shorten significantly from 0.1 mg/L to 1 mg/L, respectively (p < 0.01), accompanied by a reduced neuronal fluorescence intensity and a shortened neural axon length (p < 0.01). By 144 hpf, the motor behavior in zebrafish larvae was inhibited. Through network toxicology and molecular docking, HSP90AB1 was identified as the core target, with the cGMP/PKG signaling pathway determined to be the primary route through which BPE induces neurotoxicity in zebrafish larvae. BPE induces neuronal apoptosis and disrupts neurodevelopment by inhibiting the cGMP/PKG signaling pathway, ultimately suppressing the larval motor behavior. To further validate the experimental outcomes, we measured the expression levels of genes associated with neurodevelopment (elavl3, mbp, gap43, syn2a), serotonergic synaptic signaling (5-ht1ar, 5-ht2ar), the cGMP/PKG pathway (nos3), and apoptosis (caspase-3, caspase-9). These results offer crucial theoretical underpinnings for evaluating the ecological risks of BPE and developing environmental management plans, as well as crucial evidence for a thorough comprehension of the toxic effects and mechanisms of BPE on neurodevelopment in zebrafish larvae. Full article

In boron neutron capture therapy (BNCT), the intracellular localization and concentration of boron-10 atoms significantly influence therapeutic efficacy. Although various boronic-acid-targeted fluorescent probes have been developed to evaluate BNCT agents, most of these probes emit at short wavelengths and are, therefore, incompatible with common nuclear-staining reagents such as Hoechst 33342 and 4′,6-diamidino-2-phenylindole (DAPI). While our previously reported probe, BS-631, emitted fluorescence above 500 nm, it exhibited limitations in terms of reaction rate and fluorescence intensity. To address these issues, we developed a boronic-acid-targeted fluorescent probe with a longer emission wavelength, rapid reactivity, and strong fluorescence intensity. Herein, we designed and synthesized BTTQ, a probe based on a 2-(2-hydroxyphenyl)benzothiazole core structure. BTTQ exhibited immediate fluorescence upon reaction with 4-borono-L-phenylalanine (BPA), with an emission wavelength of 567 nm and a sufficiently high fluorescence quantum yield for detection. BTTQ quantitatively detected BPA with high sensitivity (quantification limit of 10.27 µM), suitable for evaluating BNCT agents. In addition, BTTQ exhibited selective fluorescence for BPA over metal cations. Importantly, BTTQ enabled fluorescence microscopic imaging of intracellular BPA distribution in living cells co-stained with Hoechst 33342. These results suggest that BTTQ is a promising fluorescent probe for the evaluation of future BNCT agents. Full article

A facile and versatile strategy to obtain NPs@ZnAlO nanocomposite materials, comprising controlled-size nanoparticles (NPs) within a ZnAlO matrix is reported. The mono-(Au, Ni) and bimetallic (Ni-Au) NPs serving as an active phase were prepared by the polyol-alkaline method, while the ZnAlO support was obtained via the thermal decomposition of its corresponding layered double hydroxide (LDH) precursors. X-ray diffraction (XRD) patterns confirmed the successful fabrication of the nanocomposites, including the synthesis of the metallic NPs, the formation of LDH-like structure, and the subsequent transformation to ZnO phase upon LDH calcination. The obtained nanostructures confirmed the nanoplate-like morphology inherited from the original LDH precursors, which tended to aggregate after the addition of gold NPs. According to the UV-Vis spectroscopy, loading NPs onto the ZnAlO support enhanced the light absorption and reduced the band gap energy. ATR-DRIFT spectroscopy, H₂-TPR measurements, and XPS analysis provided information about the functional groups, surface composition, and reducibility of the materials. The catalytic performance of the developed nanostructures was evaluated by the photodegradation of bisphenol A (BPA), under simulated solar irradiation. The conversion of BPA over the bimetallic Ni-Au@ZnAlO reached up to 95% after 180 min of irradiation, exceeding the monometallic Ni@ZnAlO and Au@ZnAlO catalysts. Its enhanced activity was correlated with good dispersion of the bimetals, narrower band gap, and efficient charge carrier separation of the photo-induced e⁻/h⁺ pairs. Full article

PET (polyethylene terephthalate) bottles contain different chemicals that can act as endocrine disruptors. Phthalates and bisphenol A can be found in various foods and beverages packaged in PET packaging or aluminum cans. For some phthalates, the European Union has established specified tolerable daily intakes for humans. This study aimed to establish the changes, types of phthalates (dimethyl phthalate, diethyl phthalate, diisobutyl phthalate, dibutyl phthalate, bis(2-ethylhexyl) phthalate, di-n-octyl phthalate), and bisphenol A concentrations in beer packaged in PET bottles and stored at two temperatures (4 °C and 20 °C) for four months. Beers were obtained from a local brewery after packaging into PET bottles and stored at the designated temperatures. GC-MS analysis was performed to determine phthalates and bisphenol A. Obtained data show that beers packaged in PET bottles can contain significant amounts of bisphenol A, and that their concentration increases with storage time. Phthalates were also identified in the samples, with the highest concentration of bis(2-ethylhexyl) phthalate found in the sample kept at 20 °C after 1 month of storage, sample P5; this concentration was 164.814 µg/L. BPA was recorded with the highest concentration in sample P11, which underwent 4 months of storage at a temperature of 20 °C. Full article

Bisphenols (BPs), particularly bisphenol A (BPA) and its structural analogues, are synthetic compounds widely used in plastics and industrial materials. These substances are also recognised as endocrine-disrupting chemicals (EDCs) due to their ability to interfere with hormonal systems, which has significant implications for aquatic organisms. This review summarises the occurrence, environmental distribution, and toxicity of BPs in fish, with a focus on estrogenic, androgenic, thyroid, and glucocorticoid disruptions. Studies consistently show that exposure to BPs leads to altered gene expression, developmental abnormalities, impaired reproduction, and disrupted hormonal signalling in various fish species. Although BPA alternatives like bisphenol S, bisphenol F, or bisphenol AF were introduced as safer options, emerging evidence suggests they may pose equal or greater risks. Regulatory measures are evolving, particularly within the European Union, but legislation remains limited for many bisphenol analogues. This review emphasises the need for comprehensive environmental monitoring, stricter regulatory frameworks, and the development of genuinely safer alternatives to minimise the ecological and health impacts of BPs in aquatic systems. Full article

Bisphenol A (BPA) is an endocrine-disrupting chemical with estrogen-like activity, known to impair immune function. BPA may act as a pro-inflammatory agent, reducing immune response efficacy, increasing bacterial load in E. coli infections, and altering immune responses in parasitic infections (Leishmania major, Nippostrongylus brasiliensis, Toxocara canis) through cytokine and regulatory T-cell modulation. Following its ban in food contact materials in Europe, several analogs have been introduced. This study assessed the immunotoxicity of BPA and six analogs, namely BPAP, BPE, BPP, BPS-MAE, BPZ, and TCBPA, by evaluating in vitro the antibody production. Peripheral blood mononuclear cells from healthy male and female donors were exposed to increasing concentrations of each compound for 24 h. After stimulation with rhIL-2 and ODN2006, IgM and IgG secretion were measured on day six. All compounds suppressed antibody production in a concentration-dependent manner, with some sex-related differences. IC₅₀ values showed BPP as the most potent suppressor, and BPE as the weakest. Similarly, IC₂₀ values confirmed these differences in potency, except for BPA being the weakest for IgM in males. Overall, te results do not support the idea that BPA analogs are safer than BPA. Full article

While gestational Bisphenol A (BPA) exposure has been associated with autism, limited work has focused on dietary sources. Here, we sought to develop a summary metric to capture dietary exposure specifically and test its associations with measured levels, as well as child traits related to autism. Participants (n = 116) were from the Early Autism Risk Longitudinal Investigation (EARLI) Study, which recruited pregnant women who previously had a child diagnosed with autism. Maternal concentrations of BPA were quantified in urine, and dietary sources of BPA were ascertained via food frequency questionnaires during gestation. A novel BPA “dietary burden score” was developed based on reported intake of foods known to contribute to BPA exposure (i.e., canned foods) from a Dietary History Questionnaire modified for pregnancy. Child autism-related traits were assessed via the Social Responsiveness Scale (SRS-2). We examined associations between BPA biomarkers, dietary burden scores, and child SRS scores. Dietary burden scores were weakly correlated with urinary BPA concentrations (R = 0.19, p = 0.05) but were not associated with child SRS scores. Our work suggests that more detailed dietary assessments may be needed to fully capture diet-based BPA exposures and address diet as a modifiable source of chemical exposure to reduce associated health impacts of BPA. Full article

To address the challenges posed by weak early fault signal features, strong noise interference, low diagnostic accuracy, poor reliability when using single information sources, and the limited availability of high-quality samples in practical applications for permanent magnet synchronous motor (PMSM) bearings, this paper proposes an early bearing fault diagnosis method based on Hippopotamus Optimization Variational Mode Decomposition (HO-VMD) and weighted evidence fusion of current–vibration signals. The HO algorithm is employed to optimize the parameters of VMD for adaptive modal decomposition of current and vibration signals, resulting in the generation of intrinsic mode functions (IMFs). These IMFs are then selected and reconstructed based on their kurtosis to suppress noise and harmonic interference. Subsequently, the reconstructed signals are demodulated using the Teager–Kaiser Energy Operator (TKEO), and both time-domain and energy spectrum features are extracted. The reliability of these features is utilized to adaptively weight the basic probability assignment (BPA) functions. Finally, a weighted modified Dempster–Shafer evidence theory (WMDST) is applied to fuse multi-source feature information, enabling an accurate assessment of the PMSM bearing health status. The experimental results demonstrate that the proposed method significantly enhances the signal-to-noise ratio (SNR) and enables precise diagnosis of early bearing faults even in scenarios with limited sample sizes. 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

Environmental contaminants exhibit heterogeneous neurotoxicity profiles, yet systematic comparisons between legacy neurotoxicants and emerging pollutants remain scarce. To address this gap, we implemented an integrative transcriptome meta-analysis framework that harmonized eight transcriptomic datasets spanning in vivo and in vitro neural models exposed to two legacy neurotoxicants (bisphenol A [BPA], 2, 2′, 4, 4′-tetrabromodiphenyl ether [BDE-47]) and polystyrene nanoplastics (PSNPs) as an emerging contaminant. Our analysis revealed a substantial overlap (68% consistency) in differentially expressed genes (DEGs) between BPA and PSNPs, with shared enrichment in extracellular matrix disruption pathways (e.g., “fibronectin binding” and “collagen binding”, p < 0.05). Network-based toxicogenomic mapping linked all three contaminants to six neurological disorders, with BPA showing the strongest associations with Hepatolenticular Degeneration. Crucially, a sex-stratified analysis uncovered male-specific transcriptional responses to BPA (e.g., lipid metabolism and immune response dysregulation), whereas female models showed no equivalent enrichment. This highlights the sex-specific transcriptional characteristics of BPA exposure. This study establishes a novel computational toxicology workflow that bridges legacy and emerging contaminant research, providing mechanistic insights for chemical prioritization and gender-specific risk assessment. Full article

Objective: This study aimed to assess, through a systematic review, the potential link between bisphenol A (BPA) exposure and molar incisor hypomineralization (MIH). Methods: A systematic review was performed according to the PRISMA grid. All international studies—in vitro, in vivo, or clinical—evaluating the relationships between bisphenol A and MIH were included. An iterative search of eligible publications was conducted on May 26, 2025, using three different databases: PubMed, Science Direct, and Google Scholar. Results: Eleven studies were included in the review, ten of which were experimental studies. They were published between 2013 and 2024. Among the selected articles, a rat model was used in eight studies and seven established a link between MIH and BPA (63.64% of the articles). In the included studies, the incisors of rats treated with BPA presented asymmetrical white spots at the enamel level, with a phenotype similar to human MIH. The authors highlight the hypothesis of the implication of steroid receptors expressed by ameloblasts, in particular at the stage of maturation, thus impacting enamel quality. Conclusions: The results presented in this review highlight a trend in the interaction of bisphenol A with steroid receptors, thus affecting enamel quality. However, these associations are weak, and future studies should investigate cofactors modulating BPA’s role in the development of MIH. Full article

Background/Objectives: Bisphenol A (BPA) is found throughout the environment and exposure to it has been shown to cause several health problems, including cancer. The problem with BPA is that it is a xenoestrogen that is chemically very similar to 17β-estradiol. Chronic exposure to BPA overstimulates the estrogen receptors and leads to inflammation that triggers several pathways leading to cancer progression. This is especially true in the case of hormone-sensitive breast cancers. This article reviewed the main pathways thought to be involved in the formation and/or progression of the most common forms of hormone-sensitive breast cancers due to BPA exposure. The main results were compiled and presented in tables along with a more detailed discussion of each pathway within the text. In most cases, chronic BPA exposure led to inflammation, which then triggered pathways leading to cancer stem cell formation and maintenance. In other cases, BPA exposure led to the formation of reactive oxygen species that damaged DNA and caused the formation of mutated p53 and tumorigenesis. Conclusions: The article summarizes the key pathways that are currently known, pertaining to how BPA leads to the progression and maintenance of breast cancer. The article then concludes by discussing how prenatal and perinatal BPA exposure may also predispose women to hormone-sensitive breast cancers later in life. Full article

Cardiovascular diseases (CVDs) remain the leading cause of morbidity and mortality worldwide, with increasing evidence suggesting that their origins may lie in prenatal life. Endocrine-disrupting chemicals (EDCs), such as bisphenol A (BPA), have been implicated in the alteration of fetal programming mechanisms that cause a predisposition to long-term cardiovascular vulnerability. However, the impact of prenatal endocrine disruption on fetal heart development and its sex-specific nature remains incompletely understood. This study investigates the molecular and structural effects of low-dose prenatal BPA exposure on fetal rat hearts. Our results reveal that BPA disrupts estrogen receptor (ER) signaling in a sex-dependent manner, with distinct alterations in ERα, ERβ, and GPER expression. BPA exposure also triggers significant inflammation, oxidative stress, and ferroptosis; this is evidenced by elevated NF-κB, IL-1β, TNF-α, and NLRP3 inflammasome activation, as well as impaired antioxidant defenses (SOD1, SOD2, CAT, and SELENOT), increased lipid peroxidation (MDA) and protein oxidation, decreased GPX4, and increased ACSL4 levels. These alterations are accompanied by increased markers of cardiac distension (ANP, BNP), extracellular matrix remodeling mediators, and pro-fibrotic regulators (Col1A1, Col3A1, TGF-β, and CTGF), with a more pronounced response in males. Histological analyses corroborated these molecular findings, revealing structural alterations as well as glycogen depletion in male fetal hearts, consistent with altered cardiac morphogenesis and metabolic stress. These effects were milder in females, reinforcing the notion of sex-specific vulnerability. Moreover, prenatal BPA exposure affected myocardial fiber architecture and vascular remodeling in a sex-dependent manner, as evidenced by reduced expression of desmin alongside increased levels of CD34 and Ki67. Overall, our findings provide novel insights into the crucial role of prenatal endocrine disruption during fetal heart development and its contribution to the early origins of CVD, underscoring the urgent need for targeted preventive strategies and further research into the functional impact of BPA-induced alterations on postnatal cardiac function and long-term disease susceptibility. Full article