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Bisphenol A (BPA) is an industrial pollutant that can cause immune impairment. Selenium acts as an antioxidant, as selenium deficiency often accompanies oxidative stress, resulting in organ damage. This study is the first to demonstrate that BPA and/or selenium deficiency induce pyroptosis and ferroptosis-mediated thymic injury in chicken and chicken lymphoma cell (MDCC-MSB-1) via oxidative stress-induced endoplasmic reticulum (ER) stress. We established a broiler chicken model of BPA and/or selenium deficiency exposure and collected thymus samples as research subjects after 42 days. The results demonstrated that BPA or selenium deficiency led to a decrease in antioxidant enzyme activities (T-AOC, CAT, and GSH-Px), accumulation of peroxides (H2O2 and MDA), significant upregulation of ER stress-related markers (GRP78, IER 1, PERK, EIF-2α, ATF4, and CHOP), a significant increase in iron ion levels, significant upregulation of pyroptosis-related gene (NLRP3, ASC, Caspase1, GSDMD, IL-18 and IL-1ß), significantly increase ferroptosis-related genes (TFRC, COX2) and downregulate GPX4, HO-1, FTH, NADPH. In vitro experiments conducted in MDCC-MSB-1 cells confirmed the results, demonstrating that the addition of antioxidant (NAC), ER stress inhibitor (TUDCA) and pyroptosis inhibitor (Vx765) alleviated oxidative stress, endoplasmic reticulum stress, pyroptosis, and ferroptosis. Overall, this study concludes that the combined effects of oxidative stress and ER stress mediate pyroptosis and ferroptosis in chicken thymus induced by BPA exposure and selenium deficiency.

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Endocrine disruptors such as bisphenol A (BPA) adversely affect the environment and human health. Laccases are used for the efficient biodegradation of various persistent organic pollutants in an environmentally safe manner. However, the direct application of free laccases is generally hindered by short enzyme lifetimes, non-reusability, and the high cost of a single use. In this study, laccases were immobilized on a novel magnetic three-dimensional poly(ethylene glycol) diacrylate (PEGDA)-chitosan (CS) inverse opal hydrogel (LAC@MPEGDA@CS@IOH). The immobilized laccase showed significant improvement in the BPA degradation performance and superior storage stability compared with the free laccase. 91.1% of 100 mg/L BPA was removed by the LAC@MPEGDA@CS@IOH in 3 hr, whereas only 50.6% of BPA was removed by the same amount of the free laccase. Compared with the laccase, the outstanding BPA degradation efficiency of the LAC@MPEGDA@CS@IOH was maintained over a wider range of pH values and temperatures. Moreover, its relative activity of was maintained at 70.4% after 10 cycles, and the system performed well in actual water matrices. This efficient method for preparing immobilized laccases is simple and green, and it can be used to further develop ecofriendly biocatalysts to remove organic pollutants from wastewater.

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Given the increasing concern about chemical exposure from textiles, our study examines the risks of dermal exposure to bisphenol A (BPA), bisphenol S (BPS), bisphenol B (BPB) and bisphenol F (BPF) from conventional and recycled textiles for adults, aiming to obtain new data, assess exposure, and evaluate the impact of washing on bisphenol levels. A total of 57 textile samples (33 from recycled and 24 from conventional material) were subjected to ultrasound-assisted extraction (UAE) followed by ultra-high performance liquid chromatography with tandem mass spectrometry analysis (UHPLC-MS/MS). The BPA and BPS concentrations varied widely (BPA: < 0.050 to 625 ng/g, BPS: 0.277-2,474 ng/g). The median BPA content in recycled textiles (13.5 ng/g) was almost twice as high as that of 7.66 ng/g in conventional textiles. BPS showed a median of 1.85 ng/g in recycled textiles and 3.42 ng/g in conventional textiles, indicating a shift from BPA to BPS in manufacturing practices. Simulated laundry experiments showed an overall reduction in bisphenols concentrations after washing. The study also assessed potential health implications via dermal exposure to dry and sweat-wet textiles compared to a tolerable daily intake (TDI) of 0.2 ng/kg bw/day for BPA set by the European Food Safety Authority (EFSA). Exposure from dry textiles remained below this threshold, while exposure from wet textiles often exceeded it, indicating an increased risk under conditions that simulate sweating or humidity. By finding the widespread presence of bisphenols in textiles, our study emphasises the importance of being aware of the potential risks associated with recycling materials as well as the benefits.

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Bisphenols, bisphenol A diglycidyl ether (BADGE), and bisphenol F diglycidyl ether (BFDGE) are commonly used as raw materials or additives in the production of several industrial and consumer products. However, information regarding the occurrence and distribution of these industrial chemicals in freshwater ecosystem is limited. In this study, four bisphenols, six BADGEs, and three BFDGEs were determined in abiotic and biotic samples collected from the Dongjiang River basin in southern China. Among the four bisphenols, BPA was widely present in all samples analyzed including surface water (median: 1.81 ng/L), sediment (3.1 ng/g dw), aquatic plants (3.69 ng/g dw), algae (7.57 ng/g dw), zooplankton (6.17 ng/g dw), and fish muscle (5.28 ng/g dw). Among the nine BADGEs and BFDGEs analyzed, BADGE, BADGE•H2O, BADGE·HCl·H2O and BADGE•2H2O was found in all sample types. Although the median concentration of BADGE•2H2O in surface water was below LOQ, this compound was found at median concentrations of 2.61, 3.59, 1.03, 1.69, and 49.8 ng/g dw in sediment, plants, algae, zooplankton, and fish muscle, respectively. Significant positive linear correlations were found among logarithmic transformed concentrations of BPA, BADGE, BADGE•H2O, BADGE•HCl•H2O, and BADGE•2H2O in sediment. The bioconcentration factor (logBCF) values of BADGE, BADGE•H2O, BADGE•HCl, BADGE•HCl•H2O, BADGE•2H2O, and BADGE•2HCl in fish, plants, algae, and zooplankton were > 3.3 L/kg (wet weight), indicating that these chemicals possess moderate bioaccumulation potential. The estimated daily total intake of bisphenols and BADGEs through fish consumption was 75.1 ng/kg bw/day for urban adult residents. The study provides baseline information on the occurrence of bisphenols, BADGEs, and BFDGEs in a freshwater ecosystem.

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The neurotoxicity of bisphenol A (BPA) exposure has been confirmed in vitro and in vivo, and inflammatory response is considered the main pathway. Green tea is a healthy life habit as it is rich in various anti-inflammatory components. To confirm that green tea diet is an effective measure to antagonize BPA-induced neurotoxicity, mice were treated with 0.5 and 5000 µg/kg/day of BPA from postnatal days (PNDs) 10-50 and supplemented with green tea on PND 21. From PND 51, behavioral tests were conducted on mice to assess their emotional, cognitive, and spatial learning memory capabilities. The open field test and elevated plus maze test indicated anxiety-like behaviors induced by BPA. Interestingly, green tea diet significantly alleviated BPA-induced anxiety-like behaviors. Meanwhile, the green tea diet effectively reversed BPA-induced microglia activation and morphological changes in the hippocampus of mice. Molecularly, green tea inhibited hippocampal neuroinflammation of mice by reducing BPA-induced expressions of NLRP3, ASC, cleaved-caspase-1, GSDMD-N, IL-6, and IL-1ß, as well as significantly reducing the expression of Bak1, Bax, caspase-9, and Cytc c genes (p < 0.05). Molecular docking suggests that various anti-inflammatory components of green tea can competitively bind to the estrogen receptors with BPA. In general, a green tea diet alleviates BPA-induced emotional disorders by inhibiting microglial polarization and hippocampal pyroptosis, indicating its effective antagonistic ability against the neurotoxicity induced by environmental BPA exposure.

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Bisphenols are mainly used as protective coatings for plastics and resin-based materials in various consumer products. Industrial producers have a high demand for bisphenol A (BPA) among all bisphenol substitutes for various consumer products. However, according to reports, prolonged exposure to BPA can cause multiple health issues, including neurodevelopmental disorders in young children. BPA exposure during pregnancy has been considered as the primary cause of increasing the risk of neurological disorders in children as their neural systems are designed to respond to any environmental changes during prenatal life. Recently, there has been an increased focus on the effects of prenatal exposure to BPA, as it has been found to alter gene expression related to epigenetic mechanisms like DNA methylation, histone modification, and microRNA expression. Based on the evidence, frequent interactions can lead to inherited changes in an individual's neural profile. In this review, we delve into the current knowledge regarding the toxicity mechanism of BPA for expecting mothers. Next, we will discuss the possible action of BPA on the epigenetic mechanism during brain development. This is especially important to portray an overview on the role of epigenetic modification caused by prenatal BPA exposure and next, give future directions for improving human health risk assessment caused by BPA exposure.

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Bisphenol A (BPA) is widely used around the world in the production of Polycarbonate (PC) plastics. Notably, the ubiquitous 5-gallon water bottles in the UAE are primarily made of PC plastic, making them a significant concern as bottled water is the region's main supply of drinking water. These bottles undergo temperature variations during storage and transportation, potentially leading to harmful BPA (Bisphenol A) leaching. This study analyzed 40 PC 5-gallon water bottles from two local brands A and B, with 20 bottles per brand, under two conditions: room temperature and outdoor sunlight exposure for a month. BPA levels were assessed at 0, 15, and 30 days, following ethical approval. Liquid-liquid extraction and ELISA assays were conducted, with comprehensive kit validation. The results revealed a significant increase in BPA concentration over time, particularly in bottles exposed to elevated temperatures (Day 30 outdoor-stored samples exhibited the highest concentration at 9.05 ± 2.30 µg/L). Brand B consistently exhibited higher BPA concentrations across different samples and environments. This study emphasizes the link between BPA content and storage time, highlighting the need for preventive measures to reduce BPA exposure. Individuals should be aware of potential health risks associated with prolonged storage in plastic containers and consider safer alternatives.

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Photocatalytic property of nano Ag is weak and its enhancement is important to enlarge its application. Herein, a novel strategy of constructing silver g-C3N4 biochar composite (Ag-CN@BC) as photocatalyst is developed and its photocatalytic degradation of bisphenol A (BPA) coupled with peroxydisulfate (PDS) oxidation process is characterized. Characterization result showed that silver was evenly embedded into the g-C3N4 structure of the nitrogen atoms format, impeding agglomeration of Ag by distributing stably on biochar. In optimum condition, BPA of 10 mg/L could be degraded completely at pH of 9.0 with a 0.5 g/L photocatalyst, 2 mM PDS in Ag-CN@BC-2 (Ag/melamine molar ratio of 0.5)/PDS system (99.2%, k = 4.601 h-1). Ag-CN@BC shows superior mineralization ratio in degrading BPA to CO2 and H2O via active radical way, including holes (h⁺), superoxide radicals (•O2⁻), sulfate radicals (SO4•⁻), and hydroxyl radicals (•OH). Proper amount of silver can be dispersed effectively by gC3N4, which is responsible for improving the visible-light absorbing capability and accelerate charge transfer during activation of PDS for BPA degradation, while biochar as carrier in the composite is supposed to enhance the photoelectric degradation of BPA by reducing the band gap and increasing the photocurrent of Ag-CN@BC catalyst. Ag-CN@BC exhibits excellent catalyst stability and photocatalytic activity for treatment of toxic organic contaminants in the environment.

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Bisphenol A has become a global public health problem. As an antioxidant, geraniol has potential preventive effects against toxicity. This study analyzes the preventive effect of geraniol against BPA induced liver injury in CD-1 mice. Geraniol administration significantly ameliorated BPA induced liver damage by the increase in superoxide dismutase/catalase enzymatic activities, and decrease in malonaldehyde level; prompted a significant reduction in the expression levels of inflammatory cytokines (TNF-α, IL-1ß, and IL-6), and pyroptosis biomarkers (NLRP3, ASC, and caspase-1); up-regulated the expression of claudin-1, ZO-1, and occludin markedly, which exhibited intestinal barrier function. Also, geraniol treatment optimized the composition and diversity of gut microbiota. It may be summarized that geraniol showed protective effects on liver injury induced by BPA and further revealed that the mechanism might be located on improving intestinal physical barrier function, down-regulating pyroptosis biomarkers, and normalizing intestinal microbiota, consequently reducing inflammatory response in the liver.

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In this study, visible light-activated photocatalyst oxygen-doped C3N4@Bi12O17Cl2 (OCN@BOC) and Fe(VI) coupling system was proposed for the efficient degradation of bisphenol A (BPA). The comprehensive characterization of the OCN@BOC photocatalyst revealed its excellent photogenerated carrier separation rate in heterogeneous structures. The OCN@BOC/Fe(VI)/Vis system exhibited a remarkable BPA removal efficiency of over 84% within 5 min. Comparatively, only 37% and 59% of BPA were degraded by single OCN@BOC and Fe(VI) in 5 min, respectively. Reactive species scavenging experiments, phenyl sulfoxide transformation experiments, and electron paramagnetic resonance experiments confirmed the involvement of superoxide radicals (⋅O2-), singlet oxygen (1O2), as well as iron(V)/iron(IV) (Fe(V)/Fe(IV)) species in the degradation process of BPA. Furthermore, density functional theoretical calculations and identification of intermediates provided insights into the potential degradation mechanism of BPA during these reactions. Additionally, simulation evaluations using an ecological structure activity relationship model demonstrated that the toxicity of BPA to the ecological environment was mitigated during its degradation process. This study presented a novel strategy for removing BPA utilizing visible light photocatalysts, highlighting promising applications for practical water environment remediation with the OCN@BOC/Fe(VI)/Vis system.

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A common industrial chemical known as bisphenol A (BPA) has been linked to endocrine disruption and can interfere with hormonal signaling pathways in humans and animals. This comprehensive review aims to explore the detrimental consequences of BPA on reproductive organ performance and apoptosis induction, shedding light on the emerging body of evidence from laboratory animal studies. Historically, most studies investigating the connection between BPA and reproductive tissue function have mainly leaned on laboratory animal models. These studies have provided crucial insights into the harmful effects of BPA on several facets of reproduction. This review consolidates an increasing literature that correlates exposure to BPA in the environment with a negative impact on human health. It also integrates findings from laboratory studies conducted on diverse species, collectively bolstering the mounting evidence that environmental BPA exposure can be detrimental to both humans and animals, particularly to reproductive health. Furthermore, this article explores the fundamental processes by which BPA triggers cell death and apoptosis in testicular cells. By elucidating these mechanisms, this review aids a deeper understanding of the complex interactions between BPA and reproductive tissues.

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Bisphenol A (BPA), a known endocrine disruptor, is commonly used in food containers and packaging. Recently, alternatives such as bisphenol AF (BPAF), bisphenol B (BPB), and bisphenol E (BPE) have been introduced to replace BPA. However, these substitutes have been reported to exhibit toxicity levels similar to BPA. In this study, we developed and validated a method for the analysis of trace bisphenols (BPA, BPAF, BPB, and BPE) in food using immunoaffinity column (IAC) clean-up. The method demonstrated satisfactory accuracy and precision. We applied this validated method to analyze 56 carbonated beverage samples and 30 canned tuna samples. In the carbonated beverages, average concentrations of BPA and BPAF were 0.4 and 0.2 µg kg-1, respectively. In canned tuna, BPA and BPAF were found at average concentrations of 22.2 and 0.7 µg kg-1, respectively, while BPB and BPE were not detected in any samples. Estimated exposure levels ranged from 0.13 to 0.18 ng kg bw-1 day-1 in the general population and from 205.2 to 232.0 ng kg bw-1 day-1 among consumers. The commercial IAC-based analytical method used in this study can contribute to the safety management of BPA, BPAF, BPB, and BPE.

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BACKGROUND: Hepatocellular carcinoma (HCC) remains a formidable challenge in oncology, with its pathogenesis and progression influenced by myriad factors. Among them, the pervasive organic synthetic compound, bisphenol A (BPA), previously linked with various adverse health effects, has been speculated to play a role. This study endeavors to elucidate the complex interplay between BPA, the immune microenvironment of HCC, and the broader molecular landscape of this malignancy. METHODS: A comprehensive analysis was undertaken using data procured from both The Cancer Genome Atlas and the Comparative Toxicogenomics Database. Rigorous differential expression analyses were executed, supplemented by Gene Ontology and Kyoto Encyclopedia of Genes and Genomes enrichment analyses. In addition, single-sample gene set enrichment analysis, gene set enrichment analysis and gene set variation analysis were employed to reveal potential molecular links and insights. Immune infiltration patterns were delineated, and a series of in vitro experiments on HCC cells were conducted to directly assess the impact of BPA exposure. RESULTS: Our findings unveiled a diverse array of active immune cells and functions within HCC. Distinct correlations emerged between high-immune-related scores, established markers of the tumor microenvironment and the expression of immune checkpoint genes. A significant discovery was the identification of key genes simultaneously associated with immune-related pathways and BPA exposure. Leveraging these genes, a prognostic model was crafted, offering predictive insights into HCC patient outcomes. Intriguingly, in vitro studies suggested that BPA exposure could promote proliferation in HCC cells. CONCLUSION: This research underscores the multifaceted nature of HCC's immune microenvironment and sheds light on BPA's potential modulatory effects therein. The constructed prognostic model, if validated further, could serve as a robust tool for risk stratification in HCC, potentially guiding therapeutic strategies. Furthermore, the implications of the findings for immunotherapy are profound, suggesting new avenues for enhancing treatment efficacy. As the battle against HCC continues, understanding of environmental modulators like BPA becomes increasingly pivotal.

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Halogenated bisphenol A (BPA) derivatives are produced during disinfection treatment of drinking water or are synthesized as flame retardants (TCBPA or TBBPA). BPA is considered as an endocrine disruptor especially on human follicle-stimulating hormone receptor (FSHR). Using a global experimental approach, we assessed the effect of halogenated BPA derivatives on FSHR activity and estimated the risk of halogenated BPA derivatives to the reproductive health of exposed populations. For the first time, we show that FSHR binds halogenated BPA derivatives, at 10 nM, a concentration lower than those requires to modulate the activity of nuclear receptors and/or steroidogenesis enzymes. Indeed, bioluminescence assays show that FSHR response is lowered up to 42.36 % in the presence of BPA, up to 32.79 % by chlorinated BPA derivatives and up to 27.04 % by brominated BPA derivatives, at non-cytotoxic concentrations and without modification of basal receptor activity. Moreover, molecular docking, molecular dynamics simulations, and site-directed mutagenesis experiments demonstrate that the halogenated BPA derivatives bind the FSHR transmembrane domain reducing the signal transduction efficiency which lowers the cellular cAMP production and in fine disrupts the physiological effect of FSH. The potential reproductive health risk of exposed individuals was estimated by comparing urinary concentrations (through a collection of human biomonitoring data) with the lowest effective concentrations derived from in vitro cell assays. Our results suggest a potentially high concern for the risk of inhibition of the FSHR pathway. This global approach based on FSHR activity could enable the rapid characterization of the toxicity of halogenated BPA derivatives (or other compounds) and assess the associated risk of exposure to these halogenated BPA derivatives.

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Bisphenol A (BPA), a prevalent plastic monomer and endocrine disruptor, negatively impacts metabolic functions. This study examines the chronic effects of eco-relevant BPA concentrations on hepatotoxicity, focusing on redox balance, inflammatory response, cellular energy sensors, and metabolic homeostasis in male Swiss albino mice. Chronic BPA exposure resulted in reactive oxygen species (ROS) accumulation, altered hepatic antioxidant defense, lipid peroxidation, and NOX4 expression, leading to reduced cell viability. Additionally, BPA exposure significantly upregulated hepatic pro-inflammatory cytokine genes (Tnf-α, Il-1ß, Il-6), NOS2, and arginase II, correlating with increased TLR4 expression, NF-κB phosphorylation, and a dose-dependent decrease in IκBα levels. BPA-induced NF-κB nuclear localization and inflammasome activation (NLRP3, cleaved caspase-1, IL-1ß) established an inflammatory milieu. Perturbations in hepatic AMPKα phosphorylation, SIRT1, and PGC-1α, along with elevated p38 MAPK phosphorylation and ERα expression, indicated BPA-induced energy dysregulation. Furthermore, increased PLA2G4A, COX1, COX2, and PTGES2 expression in BPA-treated livers correlated with hyperlipidemia, hepatic FASN expression, steatosis, and visceral adiposity, likely due to disrupted energy sensors, oxidative stress, and inflammasome activation. Elevated liver enzymes (ALP, AST, ALT) and apoptotic markers indicated liver damage. Notably, N-acetyl-cysteine (NAC) priming reversed BPA-induced hepatocellular ROS accumulation, NF-κB-inflammasome activation, and intracellular lipid accumulation, while upregulating cellular energy sensors and attenuating ERα expression, suggesting NAC's protective effects against BPA-induced hepatotoxicity. Pharmacological inhibition of the NF-κB/NLRP3 cascade in BAY11-7082 pretreated, or NLRP3 immunodepleted hepatocytes reversed BPA's negative impact on SIRT1/p-AMPKα/PGC-1α and intracellular lipid accumulation, providing mechanistic insights into BPA-induced metabolic disruption.

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Background: Bisphenol A (BPA), a characteristic endocrine disruptor, is a substance that seriously interferes with the human endocrine system and causes reproductive disorders and developmental abnormalities. However, its toxic effects on the gut-liver-hormone axis are still unclear. Method: Male and female rats were exposed to BPA (300 mg/kg) by oral gavage for 60 consecutive days. H&E staining was used for histopathological evaluation, and the serum biochemical indexes were determined using an automatic analyzer. The 16S rRNA gene sequencing was used to detect the intestinal microbial diversity, and the GC-MS was used to analyze the contents of short-chain fatty acids (SCFAs) in colon contents. UPLC-QTOF MS was used to analyze the related metabolites. The ELISA method was used to assess the levels of serum inflammatory factors. Results: Histopathological analysis indicated that the liver, heart, and testis were affected by BPA. There was a significant effect on alanine aminotransferase (ALT), triglyceride (TG), total cholesterol (TC), and low-density lipoprotein (LDL) in the male-BPA group (P < 0.05), and globulin (GLB), indirect bilirubin (IBIL), alkaline phosphatase (ALP), ALT, TG, TC, high-density lipoprotein (HDL), and creatinine (Cr) in the female-BPA group (P < 0.05). Metagenomics (16S rRNA gene sequencing) analysis indicated that BPA reduced the diversity and changed the composition of gut microbiota in rats significantly. Compared with the control and blank groups, the contents of caproic acid, isobutyric acid, isovaleric acid, and propanoic acid in the colon contents decreased in the male-BPA group (P < 0.05), and caproic acid, isobutyric acid, isovaleric acid, and valeric acid in the colon contents decreased in the female-BPA group (P < 0.05). Metabolomic analysis of the serum indicated that BPA could regulate bile acid levels, especially ursodeoxycholic acid (UDCA) and its conjugated forms. The contents of amino acids, hormones, and lipids were also significantly affected after exposure to BPA. The increase in interleukin-6 (IL-6), interleukin-23 (IL-23), and transforming growth factor-ß (TGF-ß) in the serum of the male-BPA group suggests that BPA exposure affects the immune system. Conclusion: BPA exposure will cause toxicity to rats via disrupting the gut-liver-hormone axis.

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Polycystic ovary syndrome (PCOS) and idiopathic hirsutism (IH) are androgen excess disorders requiring the determination of classic androgen levels for diagnosis. 11-oxygenated androgens have high androgenic potential, yet their clinical value in those disorders is not clear. Additionally, the role of endocrine disruptors (EDs), particularly in IH, remains understudied. We analyzed 25 steroids and 18 EDs in plasma samples from women with IH, PCOS, and controls using LC-MS/MS. Cytokine levels and metabolic parameters were assessed. Comparisons included non-obese women with PCOS (n = 10), women with IH (n = 12) and controls (n = 20), and non-obese versus obese women with PCOS (n = 9). Higher levels of 11-oxygenated androgens were observed in women with PCOS compared to those with IH, but not controls. Conversely, 11-oxygenated androgen levels were lower in women with IH compared to controls. Cytokine levels did not differ between women with IH and controls. Bisphenol A (BPA) levels were higher in obese women with PCOS compared to non-obese women with PCOS. Bisphenol S occurrence was higher in women with PCOS (90%) compared to controls (65%) and IH (50%). Significant correlations were found between androgens (11-ketotestosterone, androstenedione, testosterone) and insulin and HOMA-IR, as well as between immunomodulatory 7-oxygenated metabolites of DHEA and nine interleukins. Our data confirms that PCOS is a multiendocrine gland disorder. Higher BPA levels in obese women might exacerbate metabolic abnormalities. IH was not confirmed as an inflammatory state, and no differences in BPA levels suggest BPA does not play a role in IH pathogenesis.

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Bisphenol A analogues are largely used plasticisers that are going to replace bisphenol A in many sectors. Due to this replacement, their discharge and presence in the marine coastal areas are increasing, with unknown consequences for organisms and the trophic chain. This study assessed the effects of three different bisphenols (BPAF, BPF and BPS) - alone or as a mixture - provided via food (exposed clams) to the crab Carcinus aestuarii. First, clams were exposed for two weeks to 300 ng/L of each of the three bisphenols and their mixture (100 ng/L of each) to allow the bioaccumulation of the contaminants in bivalves. Then, crabs were fed for two weeks with BPA analogue-exposed clams, while unexposed clams were used to feed control crabs. After 7 and 14 days, haemolymph, gills and hepatopancreas were collected from crabs to measure a battery of biomarkers indicative of cytotoxicity, oxidative stress and damage, neurotoxicity, physiological performance (respiration and excretion rate) and electron transport system activity. Lastly, bioaccumulation of BPA analogues was assessed by UHPLC-HRMS in crabs. Our findings revealed that BPA analogue-exposed clams were able to alter total haemocyte count, haemocyte size and their proliferation. The activity of immune enzymes, such as phosphatases and phenoloxidase was altered. Moreover, we observed an impairment of antioxidant and detoxifying enzymes like SOD, CAT, GST and GPX activities. Alterations of metabolism-involved enzymes and physiological parameters and increased oxidative damage to macromolecules like proteins, lipids, and DNA were also observed in crabs. Among BPA analogues, only bioaccumulation of BPAF, which has the highest Logkow value among the tested bisphenols, was evidenced in crabs. Overall, the obtained results indicated that crabs, under the tested experimental conditions at least, underwent alterations in cellular, biochemical and physiological responses following a diet of bisphenol-exposed clams, suggesting a potential ecotoxicological risk in the marine food chain.

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Bisphenol A (BPA), chemically known as 2,2-bis(4-hydroxyphenyl) propane, is one of the most common endocrine-disrupting chemicals in our environment. Long-term or high-dose exposure to BPA may lead to testicular damage and adversely affect male reproductive function. In vivo studies on rodents have demonstrated that BPA triggers apoptosis in testicular cells through both intrinsic and extrinsic pathways. Further in vitro studies on spermatogonia, Sertoli cells, and Leydig cells have all confirmed the pro-apoptotic effects of BPA. Given these findings, apoptosis is considered a primary mode of cell death induced by BPA in testicular tissue. In addition, BPA promotes autophagy by altering the activity of the Akt/mTOR pathway and upregulating the expression of autophagy-related genes and proteins. Recent studies have also identified ferroptosis as a significant contributing factor to BPA-induced testicular damage, further complicating the landscape of BPA's effects. This review summarizes natural substances that mitigate BPA-induced testicular damage by inhibiting these cell death pathways. These findings not only highlight potential therapeutic strategies but also underscore the need for further research into the underlying mechanisms of BPA-induced toxicity, particularly as it pertains to human health risk assessment and the development of more effective BPA management strategies.

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This study explored Mason pine-derived hydrochar (MPHC) as an effective adsorbent and persulfate (PS) activator for degrading bisphenol A (BPA). Increasing MPHC dosage from 0.25 to 2.0 g L-1 raised BPA removal from 42% to 87%. Similarly, at the same MPHC dosage range and fixed PS concentration (8 mM), BPA removal by MPHC/PS increased from 66% to 91%. Additionally, at a fixed MPHC dosage (1.0 g L-1), higher PS concentrations (2-32 mM) resulted in an overall BPA removal increase from 78% to 99%. The optimal pH for BPA removal by MPHC was at pH 3, while for MPHC/PS was at pH 9. BPA degradation by MPHC was optimal at pH 3, whereas MPHC/PS was at pH 3 and pH 9. Additionally, pH 7 favored BPA adsorption for both MPHC and MPHC/PS. The study also considered the influence of coexisting anions and humic acid (HA). PO43- and NO3- influence adsorption on MPHC, but these anions' effect on MPHC/PS is limited. Furthermore, the existence of HA had minimal influence on BPA removal by MPHC/PS. The contributions of different reactive species by MPHC for BPA degradation are as follows: electron-hole (h+) 2%, singlet oxygen (1O2) 7%, superoxide radicals (O2•-) 13%, electron (e-) 2%, hydroxyl radical (•OH) 3%, whereas the remaining 48% removal was the contribution of adsorption. For MPHC/PS, adsorption accounted for 39 %, more reactive species were involved in degradation, and the donations are (h+) 3%, sulfate radicals (SO4•-) 3%, (1O2) 19%, (O2•-) 15%, (e-) 2%, and (•OH) 2%. Additionally, the performance of MPHC remains stable after three operational cycles. The preparation cost of MPHC is 3.01 € kg-1. These results highlight the potential of MPHC as an environmentally friendly material for activating PS and removing organic pollutants, suggesting its promising application in future environmental remediation efforts.