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In this presented study, the aim was to investigate the toxic effects of bisphenol S (BPS), one of the bisphenol A analogues, on the thyroid glands of male Wistar albino rats. Toward this aim, the rats (n = 28) were given a vehicle (control) or BPS at 3 different doses, comprising 20, 100, and 500 mg/kg of body weight (bw) via oral gavage for 28 days. According to the results, BPS led to numerous histopathological changes in the thyroid tissue. The average proliferation index values among the thyroid follicular cells (TFCs) displayed increases in all of the BPS groups, and significant differences were observed in the BPS-20 and BPS-100 groups. The average apoptotic index values in the TFCs were increased significantly in the BPS-500 group. The serum thyroid-stimulating hormone and serum free thyroxine levels did not show significant changes after exposure to BPS; however, the serum free triiodothyronine levels displayed significant decreases in all 3 of the BPS groups. BPS was determined to cause significant increases in the antioxidant enzyme activities of catalase, superoxide dismutase, glutathione-S-transferase, glutathione peroxidase, as well as a significantly decreased content of reduced glutathione. The malondialdehyde level in the thyroid tissue was elevated significantly in the BPS-500 group. The data obtained herein revealed that BPS has thyroid-disrupting potential based on structural changes, follicle cell responses, and biochemical alterations including a decreased serum free triiodothyronine level and increased oxidative stress. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

Water pollution has emerged as a critical global challenge, particularly the contamination of water bodies with persistent organic pollutants such as Bisphenol S (BPS), a known endocrine disruptor. This study presents the synthesis and application of eco-friendly bio-based coconut shell magnetic biochar (CSMB) for efficient sequestration of BPS from aqueous environments. Utilizing pyrolysis and co-precipitation techniques, the magnetic biochar was characterized through various methods including surface chemistry (pHpzc), electron dispersive X-ray analysis (EDX), Brunauer-Emmett-Teller (BET) N2 adsorption-desorption, scanning electron microscopy (SEM), vibrating sample magnetometer (VSM), and Fourier transform infrared spectroscopy (FTIR). SEM revealed a porous structure with a high surface area, while FTIR confirmed the presence of functional groups essential for adsorption. X-ray diffraction (XRD) and VSM successfully incorporated magnetic nanoparticles, enhancing the separation process post-adsorption. The CSMB demonstrated a significant surface area of 373 m2 g−1, outperforming regular coconut shell biochar (CSB), with a BPS adsorption capacity of 43.5 mg/g compared to 26.7 mg/g for CSB. Batch adsorption tests assessed the impact of operational factors such as initial BPS concentration (8–150 ppm), contact time (30–150 min), temperature (298.15, 318.15, and 338.15 K), pH (3–11), and CSMB dosage (0.1–0.9 g). The results indicated optimal adsorption at pH 6 with a maximum capacity of 52.3 mg/g. Kinetic studies revealed that the pseudo-second-order model best described the adsorption process, while the Langmuir isotherm model provided an excellent fit for the adsorption data. The reusability of CSMB was validated over five cycles, with adsorption capacity decreasing slightly from 43.5 mg/g to approximately 41 mg/g, making it a sustainable and effective adsorbent for water treatment. [ABSTRACT FROM AUTHOR]

Bisphenols are widely used in the manufacture of polycarbonates and plastics. With the restriction and banning of bisphenol A (BPA), a typical representative of bisphenols, bisphenol S (BPS) has been widely used in the manufacture of various polymers as the main alternative to BPA. Humans are exposed to BPS through a variety of routes, and BPS is detected in food, environment, and human blood and excreta. Concerns about the safety of BPS have become an important issue, especially for pregnant women and fetuses. The results of several studies support that prenatal exposure to BPS have multiple adverse effects on the offspring. In particular, prenatal BPS exposure may affect maternal and offspring metabolic homeostasis and increase the risk of abnormal lipid metabolism in the offspring. This paper summarized the results of studies on BPS exposure and abnormal lipid metabolism. In addition, this review explored potential mechanisms of BPS, including its possible influence on lipid metabolism through interference with hormone receptors, activation of the nuclear receptor peroxisome proliferator-activated receptor γ (PPARγ), induction of oxidative stress and inflammatory states, and epigenetic effects. These findings emphasized the importance of more in-depth research on BPS and its potential effects to better understand its impact on human health and to provide a basis for developing appropriate public health measures to reduce the risk of BPS exposure.

Abstract Background Bisphenol S (BPS) is a substitute for bisphenol A in plastic manufacturing and, as a potential endocrine disruptor, may alter the physiology of the oviduct, in which fertilization and early embryo development take place in mammals. The objective of this study was to assess the effect of a daily dietary exposure to BPS combined with a contrasted diet on the oviduct fluid proteome using an ovine model. Results Eighty adult cyclic ewes were allotted to four groups (20/group): overfed (OF) consuming 50 µg/kg/day of BPS in their diet, underfed (UF) consuming 50 µg/kg/day of BPS, and non-exposed controls in each diet group. After three months, the mean body condition score, plasma levels of glucose and non-esterified fatty acids were significantly higher in OF than in UF females. The proteins in collected OF samples (50 µg) were analyzed by nanoliquid chromatography coupled with tandem mass spectrometry (nanoLC-MS/MS). Overall, 1563 proteins were identified, among which 848 were quantified. Principal component analysis of the data revealed a clear discrimination of samples according to the diet and a segregation between BPS-exposed and non-exposed females in overfed ewes. Hierarchical clustering of differentially abundant proteins (DAPs) identified two clusters of 101 and 78 DAPs according to the diet. Pairwise comparisons between groups revealed a stronger effect of BPS in OF than in UF females (70 vs. 24 DAPs) and a stronger effect of the diet in BPS-exposed than non-exposed females (56 vs. 36 DAPs). Functional analysis of DAPs showed an enrichment in metabolic processes, immune system, cell response to stress, and reproductive processes. Conclusions This work highlights for the first time the important impact of BPS on the oviduct proteome, with larger effects seen in OF than UF females. These results, together with previous ones, raise health concerns for everyone and call for a greater regulation of BPS in the food industry.

AbstractAs an alternative to bisphenol A (BPA), bisphenol S (BPS) has been used as an ink developer in thermal paper products including price labels on food packaging which have been suggested as the sources of BPS found at high levels in packaged fish samples. BPS in the printed price labels glued onto the outside of plastic film could migrate indirectly from the printed surface through the paper, adhesive and film into the food. In order to investigate if price labels could also be the sources of BPS detected in the meat samples in our previous studies, meat and other food samples packaged under different conditions were collected, and BPS in these samples together with the price labels on the corresponding packaging were extracted with solvent followed by solid phase extraction and stable isotope dilution LC-MS/MS analysis. BPS was detected at very high levels (161.7–222.4 µg/cm2) in all the five sticker type of price labels, indicating BPS being the dominant if not the sole ink developer. BPS was also detected in all the 26 continuous roll type of price labels but at very low levels (0.017–18 ng/cm2), indicating that the dominant ink developer is likely one of the other alternatives, rather than BPS. Despite BPS being detected in all price labels on packaging of fish, meat, and cheese samples, BPS was not detected or detected in only a few fish, meat, and cheese samples at levels considerably lower than the current EU specific migration limit (SML) of 50 ng/g food for BPS authorised under Regulation (EU) 10/2011. [ABSTRACT FROM AUTHOR]

Thyroid hormones play a crucial role in numerous physiological processes, including reproduction. Bisphenol S (BPS) is a structural analog of Bisphenol A known for its toxic effects. Interference of this substitute with normal thyroid function has been described. To investigate the effect of thyroid disruption on ovarian development following maternal exposure to BPS, female rats were exposed, daily, to either AT 1–850 (a thyroid hormone receptor antagonist) (10 nmol/rat) or BPS (0.2 mg/kg) during gestation and lactation. The effects on reproductive outcome, offspring development, histological structures, hormone levels, oxidative status, cytoskeleton proteins expression, and oocyte development gene expression were examined. Our results are in favor of offspring ovarian development disruption due to thyroid disturbance in adult pregnant females. During both fetal and postnatal stages, BPS considerably altered the histological structure of the thyroid tissue as well as oocyte and follicular development, which led to premature ovarian failure and stimulation of oocyte atresia, being accompanied with oxidative stress, hypothalamic-pituitary-ovarian axis disorders, and cytoskeletal dynamic disturbance. Crucially, our study underscores that BPS may induce reproductive toxicity by blocking nuclear thyroid hormone receptors, evidenced by the parallelism and the perfect meshing between the data obtained following exposure to AT 1–850 and those after the treatment by this substitute. [ABSTRACT FROM AUTHOR]

Bisphenols are endocrine-disrupting chemicals used in plastics and resins for food packaging. This study aimed to evaluate the exposure to bisphenol A (BPA), bisphenol S (BPS), and bisphenol F (BPF) associated with the consumption of fresh, canned, and ready-to-eat meals and determine the effects of bisphenols on blood pressure and heart rate. Forty-eight healthy young adults were recruited for this study, and they were divided into the following three groups: fresh, canned, and ready-to-eat meal groups. Urine samples were collected 2, 4, and 6 h after meal consumption, and blood pressure and heart rate were measured. The consumption of ready-to-eat meals significantly increased urine BPA concentrations compared with canned and fresh meal consumption. No significant difference in BPS and BPF concentrations was observed between the groups. The consumption of ready-to-eat meals was associated with a significant increase in systolic blood pressure and pulse pressure and a marked decrease in diastolic blood pressure and heart rate. No significant differences were noted in blood pressure and heart rate with canned and fresh meal consumption. It can be concluded that total BPA concentration in consumed ready-to-eat meals is high. High BPA intake causes increase in urinary BPA concentrations, which may, in turn, lead to changes in some cardiovascular parameters. [ABSTRACT FROM AUTHOR]

Background: Prenatal bisphenol exposure has been reported to be associated with lower birth weight and obesity-related indicators in early childhood. These findings warrant an investigation of the relationship between prenatal bisphenol exposure and the dynamic growth of offspring. This study aimed to evaluate the relationship of maternal bisphenol concentration in urine with the body mass index (BMI) growth trajectory of children aged up to two years and to identify the critical exposure periods. Methods: A total of 826 mother–offspring pairs were recruited from Wuhan Children's Hospital between November 2013 and March 2015. Maternal urine samples collected during the first, second, and third trimesters were analyzed for bisphenol A (BPA), bisphenol S, and bisphenol F (BPF) concentrations. Measurements of length and weight were taken at 0, 1, 3, 6, 8, 12, 18, and 24 months. Children's BMI was standardized using the World Health Organization reference, and group-based trajectory modeling was used to identify BMI growth trajectories. The associations between prenatal bisphenol exposure and BMI growth trajectory patterns were assessed using multinomial logistic regression models. Results: The BMI growth trajectories of the 826 children were categorized into four patterns: low-stable (n = 134, 16.2%), low-increasing (n = 142, 17.2%), moderate-stable (n = 350, 42.4%), and moderate-increasing (n = 200, 24.2%). After adjusting for potential confounders, we observed that prenatal exposure to BPA during the second trimester [odds ratio (OR) = 2.20, 95% confidence interval (CI) = 1.09–4.43] and BPF during the third trimester (OR = 3.28, 95% CI = 1.55–6.95) at the highest quartile concentration were associated with an increased likelihood of the low-increasing BMI trajectory. Furthermore, in the subgroup analysis by infant sex, the positive association between the highest quartile of prenatal average urinary BPF concentration during the whole pregnancy and the low-increasing BMI trajectory was found only in girls (OR = 2.82, 95% CI = 1.04–7.68). Conclusion: Our study findings suggest that prenatal exposure to BPA and BPF (a commonly used substitute for BPA) is associated with BMI growth trajectories in offspring during the first two years, increasing the likelihood of the low-increasing pattern. 3m5uKxpSj9JCA5GegjWbHb Video Abstract (MP4 120033 kb) [ABSTRACT FROM AUTHOR]

Background: Bisphenol S (BPS) is a substitute for bisphenol A in plastic manufacturing and, as a potential endocrine disruptor, may alter the physiology of the oviduct, in which fertilization and early embryo development take place in mammals. The objective of this study was to assess the effect of a daily dietary exposure to BPS combined with a contrasted diet on the oviduct fluid proteome using an ovine model. Results: Eighty adult cyclic ewes were allotted to four groups (20/group): overfed (OF) consuming 50 µg/kg/day of BPS in their diet, underfed (UF) consuming 50 µg/kg/day of BPS, and non-exposed controls in each diet group. After three months, the mean body condition score, plasma levels of glucose and non-esterified fatty acids were significantly higher in OF than in UF females. The proteins in collected OF samples (50 µg) were analyzed by nanoliquid chromatography coupled with tandem mass spectrometry (nanoLC-MS/MS). Overall, 1563 proteins were identified, among which 848 were quantified. Principal component analysis of the data revealed a clear discrimination of samples according to the diet and a segregation between BPS-exposed and non-exposed females in overfed ewes. Hierarchical clustering of differentially abundant proteins (DAPs) identified two clusters of 101 and 78 DAPs according to the diet. Pairwise comparisons between groups revealed a stronger effect of BPS in OF than in UF females (70 vs. 24 DAPs) and a stronger effect of the diet in BPS-exposed than non-exposed females (56 vs. 36 DAPs). Functional analysis of DAPs showed an enrichment in metabolic processes, immune system, cell response to stress, and reproductive processes. Conclusions: This work highlights for the first time the important impact of BPS on the oviduct proteome, with larger effects seen in OF than UF females. These results, together with previous ones, raise health concerns for everyone and call for a greater regulation of BPS in the food industry. [ABSTRACT FROM AUTHOR]

Bisphenol S (BPS) is widely presented and affects aging with unclear mechanisms. Here, we applied C. elegans to evaluate the effects of BPS on lifespan and healthspan and to investigate the underlying mechanisms. Both early-life and whole-life exposure to BPS at environmentally relevant doses (0.6, 6, 60 μg/L) significantly decreased lifespan, and healthspan (body bend, pharyngeal pumping, and lipofuscin accumulation). BPS exposure impaired mitochondrial structure and function, which promoted ROS production to induce oxidative stress. Furthermore, BPS increased expressions of the insulin/IGF-like signaling (IIS). Also, BPS inhibited expression of the IIS transcription factor daf-16 and its downstream anti-oxidative genes. Quercetin effectively improved BPS-induced oxidative stress byreversing BPS-regulated IIS/daf-16 pathway and anti-oxidative gene expressions. In daf-2 and daf-16 mutants, the effects of BPS and quercetin on lifespan, healthspan, oxidative stress, and anti-oxidative genes expressions were reversed, demonstrating the requirement of IIS/daf-16 for aging regulation. Molecular docking and molecular dynamics simulations confirmed the stable interaction between DAF-2 and BPS mainly via three residues (VAL1260, GLU1329, and MET1395), which was attenuated by quercetin. Our results highlighted that adverse effects of BPS on impairing lifespan and healthspan by affecting IIS/daf-16 function against mitochondrial stress, which could be inhibited by quercetin treatment. Thus, we first revealed the underlying mechanisms of BPS-induced aging and the potential treatment.

Owing to its capacity to damage the endocrine system, bisphenol A (BPA) is being substituted in common consumer products by chemically related compounds, including bisphenol F (BPF) and bisphenol S (BPS). Although BPF and BPS in body fluids are comparable in concentration and frequency to BPA, the toxicity of these analogs in female reproduction remains largely unknown. Using a nontargeted metabolomics technique, this study aimed to examine the effect of BPF and BPS exposure on the metabolism of human ovarian granulosa (KGN) cells. Analysis of the differentially expressed metabolites (DEMs) identified 991 and 609 DEMs in the KGN cells exposed to BPF and BPS, respectively, at three various concentrations (0.1, 1, and 10 µM), with BPF having a greater interfering effect than BPS. Specifically, exposure to low concentrations (0.1 µM) of both bisphenols more greatly affected cellular metabolism than exposure to higher concentrations. Metabolic pathway enrichment analysis using the KEGG database revealed that the mechanisms by which BPF and BPS induced toxicity in the granulosa cells were different: BPF exposure significantly altered purine metabolism, autophagy-related pathways, and ferroptosis, whereas BPS mainly interfered with one-carbon metabolism (vitamin B6, riboflavin, and folate). These results demonstrated the differences in the mechanisms by which BPF and BPS induced to granulosa cell dysfunction.

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Research on thermal receipts has previously focused on the toxic effects of dermal exposure from the most publicized developers (e.g., bisphenol A (BPA) and bisphenol S (BPS)), while no studies have reported on the other solvent-extractable compounds therein. Diphenyl sulfone (DPS) is a sensitizer added to thermal receipts, but little is known about DPS concentrations in receipts or potential toxicity. Here, we quantified BPA, BPS, and DPS concentrations and tentatively identified the solvent-extractable compounds of thermal receipts collected from three South Dakota (USA) cities during 2016–2017. An immortalized chicken hepatic cell line, cultured as 3D spheroids, was used to screen effects of DPS, BPS, and 17ß estradiol (E2; 0.1–1000 µM) on cell viability and gene expression changes. These chemicals elicited limited cytotoxicity with LC50 values ranging from 113 to 143 µM, and induced dysregulation in genes associated with lipid and bile acid homeostasis. Taken together, this study generated novel information on solvent-extractable chemicals from thermal receipts and toxicity data for DPS. [ABSTRACT FROM AUTHOR]

Suaeda glauca (SG), widely applied to restore salinized land, was used to prepare biochar (activated) for the adsorption of bisphenol S (BPS) from water. SG had a high cellulose content and uniform salt ion distribution. The migration pathway of salt ions in halophytes was analyzed via energy dispersive spectrometer (EDS), inductively coupled plasma atomic emission spectrometry (ICP-AES), and X-ray diffraction (XRD). Phosphoric acid impregnation could lead to the leaching of 80.52% of salt ions from SG. The products had high specific surface area (1339 m2/g) and adsorption capacity for BPS (437 mg/g). Response surface methodology indicated that pH and temperature could significantly influence the adsorption capacity. Molecular dynamics and quantum chemistry were used to describe the adsorption process and mechanism. By comparing the pore size distribution and adsorption capacity of different carbons with the simulation results of molecular dynamics, it can be discovered that the effect of micropore size on pollutant adsorption is verifiable through graphite layer modeling. Meanwhile, the presence of salt ions had no significant effect on BPS adsorption capacity. The absorption mechanism might be ascribed to a large specific surface area and π–π bond interactions. [ABSTRACT FROM AUTHOR]

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.

Bisphenol is a chemical substance widely used in plastic products and food containers. In this study, we observed a relationship between DNA methylation and atopic dermatitis (AD) in the peripheral blood mononuclear cells (PBMCs) of pregnant women exposed to bisphenol A (BPA) and its alternatives, bisphenol S (BPS) and bisphenol F (BPF). DNA methylation is an epigenetic mechanism that regulates gene expression, which can be altered by environmental factors, and affects the onset and progression of diseases. We found that genes belonging to the JAK-STAT and PI3K-AKT signaling pathways were hypomethylated in the blood of pregnant women exposed to bisphenols. These genes play important roles in skin barrier function and immune responses, and may influence AD. Therefore, we suggest that not only BPA, but also BPS and BPF, which are used as alternatives, can have a negative impact on AD through epigenetic mechanisms. [ABSTRACT FROM AUTHOR]

Bisphenol A (BPA) and its structural analogs (bisphenol S (BPS) and bisphenol F (BPF)) are widely consumed endocrine disrupting chemicals that may contribute to the etiology of obesity. To date, few studies have directly investigated the sex-related associations between bisphenols and body fat distribution in adults. In this study, we included 2669 participants from the National Health and Nutrition Examination Survey (NHANES) 2011–2016 to evaluate and compare sex-specific differences of the associations of BPA, BPS, and BPF with body fat distribution. We found that there were significant positive correlations between BPS and body fat indices (STFAT [adjustedβ=1.94, 95% CI: (0.24, 3.64)], TAF [0.18 (0.04, 0.32)], SAT [0.15 (0.03, 0.27)], android fat mass [0.20 (0.004, 0.40)], BMI [1.63 (0.61, 2.65)], and WC [3.19 (0.64, 5.73)] in the highest quartiles of BPS), but not in BPA and BPF. Stratified analyses suggested that the significant associations of BPS with body fat indices were stronger in women than men (STFAT [adjustedβ=3.75, 95% CI: (1.04, 6.45) vs. adjustedβ=−0.06, 95% CI: (−2.23, 2.11), P for interaction < 0.001], TAF [ 0.32 (0.09, 0.54) vs. 0.01 (−0.17, 0.19), P for interaction < 0.001], SAT [0.27 (0.09, 0.45) vs. 0.01 (−0.14, 0.16), P for interaction < 0.001], android fat mass [0.41 (0.12, 0.71) vs. −0.02 (−0.28, 0.24), P for interaction < 0.001], gynoid fat mass [0.56 (0.11, 1.01) vs. −0.05 (−0.41, 0.31), P for interaction = 0.002], BMI [2.76 (1.08, 4.44) vs. 0.47 (−0.80, 1.74), P for interaction < 0.001], and WC [5.51 (1.44, 9.58) vs. 0.61 (−2.67, 3.88), P for interaction < 0.001]), and positive associations between BPS with fat distribution were also observed in non-smoking women. Our study indicated that in women, higher concentration of urinary BPS was associated with increased body fat accumulation, except for visceral adipose tissue mass. These findings emphasize the role of environmental BPS exposure in the increasing fat deposits, and confirm the need for more prospective cohort studies on a sex-specific manner. [ABSTRACT FROM AUTHOR]

The study aimed to investigate the underlying molecular mechanisms of prostate injury induced by 4,4′‐sulfonyldiphenol (BPS) exposure and propose a novel research strategy to systematically explore the molecular mechanisms of toxicant‐induced adverse health effects. By utilizing the ChEMBL, STITCH, and GeneCards databases, a total of 208 potential targets associated with BPS exposure and prostate injury were identified. Through screening the potential target network in the STRING database and Cytoscape software, we determined 21 core targets including AKT1, EGFR, and MAPK3. Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses conducted through the DAVID database illustrated that the potential targets of BPS in prostatic toxicity were primarily enriched in cancer signaling pathways and calcium signaling pathways. These findings suggest that BPS may actively participate in the occurrence and development of prostate inflammation, prostatic hyperplasia, prostate cancer, and other aspects of prostate injury by regulating prostate cancer cell apoptosis and proliferation, activating inflammatory signaling pathways, and modulating prostate adipocytes and fibroblasts. This research provides a theoretical basis for understanding the molecular mechanism of underlying BPS‐induced prostatic toxicity and establishes a foundation for the prevention and treatment of prostatic diseases associated with exposure to plastic products containing BPS and certain BPS‐overwhelmed environments. This study aimed to investigate the mechanism of 4,4′‐sulfonyldiphenol (BPS)‐mediated prostate injury and explore a new approach to understanding the molecular mechanisms of toxicants based on network toxicology. Potential targets of BPS‐induced prostate injury were obtained from databases and core targets were screened using network analysis. The results showed that BPS mediated prostatic toxicity mainly through cancer and calcium signaling pathway. This research provides a theoretical basis for understanding BPS‐induced prostatic toxicity and lays foundation for its prevention and treatment. [ABSTRACT FROM AUTHOR]

Simple Summary: In recent years, authoritative journals have consistently reported DHODH's critical role in resistance to ferroptosis, significantly advancing the research on related mechanisms. Nevertheless, the nucleotide sequence of the yak DHODH gene remains unknown, and its involvements in ferroptosis processes in yak cells remain elusive. Therefore, in the present study, we cloned the coding region of the yak DHODH gene, and revealed its high conservation in mammals. Furthermore, by using a bisphenol S (BPS)-induced ferroptosis model, we confirmed the role of the DHODH gene in mitigating ferroptosis in yak skin fibroblasts (YSFs) derived from a three-mouth-old fetus. This study offers theoretical support for further exploring the functions of the yak DHODH gene and partially elucidating the molecular mechanisms underlying ferroptosis. Dihydroorotate dehydrogenase (DHODH) is a rate-limiting enzyme of de novo biosynthesis of pyrimidine. Although the involvement of DHODH in resisting ferroptosis has been successively reported in recent years, which greatly advanced the understanding of the mechanism of programmed cell death (PCD), the genetic sequence of the yak DHODH gene and its roles in ferroptosis are still unknown. For this purpose, we firstly cloned the coding region sequence of DHODH (1188 bp) from yak liver and conducted a characterization analysis of its predictive protein that consists of 395 amino acids. We found that the coding region of the yak DHODH gene presented high conservation among species. Second, the expression profile of the DHODH gene in various yak tissues was investigated using RT-qPCR. The results demonstrated that DHODH was widely expressed in different yak tissues, with particularly high levels in the spleen, heart, and liver. Third, to investigate the involvement of DHODH in regulating ferroptosis in cells, yak skin fibroblasts (YSFs) were isolated from fetuses. And then, bisphenol S (BPS) was used to induce the in vitro ferroptosis model of YSFs. We observed that BPS decreased the cell viability (CCK8) and membrane potential (JC-1) of YSFs in a dose-dependent manner and induced oxidative stress by elevating reactive oxygen species (ROS). Simultaneously, it was evident that BPS effectively augmented the indicators associated with ferroptosis (MDA and BODIPY staining) and reduced GSH levels. Importantly, the co-administration of Ferrostatin-1 (Fer), a potent inhibitor of ferroptosis, significantly alleviated the aforementioned markers, thereby confirming the successful induction of ferroptosis in YSFs by BPS. Finally, overexpression plasmids and siRNAs of the yak DHODH gene were designed and transfected respectively into BPS-cultured YSFs to modulate DHODH expression. The findings revealed that DHODH overexpression alleviated the occurrence of BPS-induced ferroptosis, while interference of DHODH intensified the ferroptosis process in YSFs. In summary, we successfully cloned the coding region of the yak DHODH gene, demonstrating its remarkable conservation across species. Moreover, using BPS-induced ferroptosis in YSFs as the model, the study confirmed the role of the DHODH gene in resisting ferroptosis in yaks. These results offer valuable theoretical foundations for future investigations into the functionality of the yak DHODH gene and the underlying mechanisms of ferroptosis in this species. [ABSTRACT FROM AUTHOR]

The plastic additive bisphenol S (BPS) has been widely used in various industrial and household products, and frequently detected in environmental and human samples. For the past few years, increasing concern has been focused on the visual toxicity of BPS. Here, after zebrafish embryos were exposed to BPS (1, 10, 100, and 1 000 μg·L-1) for 15 days, retinal histology and expression of genes involved in retinoic acid metabolism and opsin genes were examined to investigate the effect of BPS on the early visual development of larval zebrafish. The results showed that exposure to 10, 100 and 1 000 μg·L-1 BPS inhibited the expression of genes related to retinoic acid synthesis and the expression of neural retina leucine zipper gene (nrl) that related to photoreceptor cell development, while the expression of opsin genes (zfblue, zfuv and zfgr) was increased in 100 μg·L-1 and 1 000 μg· L-1 BPS groups. The results of hematoxylin-eosin staining showed that the thickness of the retina, the ganglion cell layer, the inner nuclear layer, and the outer nuclear layer was significantly decreased by different doses of BPS. In addition, BPS also induced small eyes in 15-dpf zebrafish larvae, based on Pearson correlation analysis of the body length, the head width, and the eye diameter. In summary, our study suggested that BPS probably affected early retinal development of zebrafish by interfering with retinoic acid metabolism, and its potential health risk to the visual system should arouse extensive attention. [ABSTRACT FROM AUTHOR]

Exposure to bisphenol S (BPS) is known to adversely affect neuronal development. As pivotal components of neuronal polarization, axons and dendrites are indispensable structures within neurons, crucial for the maintenance of nervous system function. Here, we investigated the impact of BPS exposure on axonal and dendritic development both in vivo and in vitro. Our results revealed that exposure to BPS during pregnancy and lactation led to a reduction in the complexity, density, and length of axons and dendrites in the prefrontal cortex (PFC) of offspring. Employing RNA sequencing technology to elucidate the underlying mechanisms of axonal and dendritic damage induced by BPS, Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis highlighted a significant alteration in the oxidative phosphorylation (OXPHOS) pathway, essential for mitochondrial function. Subsequent experiments demonstrate BPS-induced impairment in mitochondrial function, including damaged morphology, decreased adenosine triphosphate (ATP) and superoxide dismutase (SOD) levels, and increased reactive oxygen species and malondialdehyde (MDA). These alterations coincided with the downregulated expression of OXPHOS pathway-related genes (ATP6V1B1, ATP5K, NDUFC1, NDUFC2, NDUFA3, COX6B1) and Myosin 19 (Myo19). Notably, Myo19 overexpression restored the BPS-induced mitochondrial dysfunction by alleviating the inhibition of OXPHOS pathway. Consequently, this amelioration was associated with a reduction in BPS-induced axonal and dendritic injury observed in cultured neurons of the PFC.

Background: Bisphenol A (BPA) is known as an obesogenic endocrine disruptor. Bisphenol S (BPS) and F (BPF) are substitutes that have recently replaced BPA. Objectives: To investigate the relationships of urinary bisphenols (BPA, BPS and BPF) with adiposity measurements (obesity, BMI z-score, and fat mass), serum adipokine levels (adiponectin and leptin), and adiponectin/leptin ratio (A/L ratio) in 6- and 8-year-old children. Methods: A total of 561 children who participated in the Environment and Development of Children cohort (482 and 516 children visited at age 6 and 8, respectively) at Seoul National University Children’s Hospital during 2015–2019 were included. Urinary BPA levels were log-transformed. BPS levels were categorized into three groups (non-detected, lower-half, and higher-half of detected), and BPF levels were classified into two groups (non-detected and detected). Results: The urinary BPS higher-half group had a higher BMI z-score (β = 0.160, P = 0.044), higher fat mass (β = 0.104, P < 0.001), lower adiponectin concentration (β =- 0.069, P < 0.001), higher leptin concentration (β = 0.360, P < 0.001), and lower A/L ratio (β =- 0.428, P < 0.001) compared with the non-detected group. The urinary BPF-detected group had a higher fat mass (β = 0.074, P < 0.001), lower adiponectin concentration (β =- 0.069, P < 0.001), higher leptin concentration (β = 0.360, P < 0.001), and lower A/L ratio (β =- 0.428, P < 0.001) compared with the non-detected group. The BPA levels showed no consistent associations with outcomes, except for isolated associations of BPA at age 6 with a higher BMI z-score at age 6 (P = 0.016) and leptin at age 8 (P = 0.021). Conclusions: Increased exposure to BPS and BPF is associated with higher fat mass and leptin concentration, lower serum adiponectin, and lower A/L ratio in children. These findings suggest potential adverse effects of BPA substitutes on adiposity and adipokines. No consistent association of BPA exposure with outcomes could be partly explained by the decreasing BPA levels over time.

Bisphenol A (BPA) and its substitute bisphenol S (BPS) are desirable materials widely used in manufacturing plastic products but can pose carcinogenic risks to humans. A new conductive iron-based metal-organic framework (Fe-HHTP)-modified pencil graphite electrode (PGE) for electrochemically sensing BPA and BPS was prepared and fully characterized by SEM, TEM, FT-IR, XRD, and XPS. Results showed that the optimal conditions for preparing Fe-HHTP/PGE were a pH of 6.5, a Fe-HHTP concentration of 2 mg·mL−1, a deposition potential of 0 V, and a deposition time of 100 s. The Fe-HHTP/PGE prepared under such conditions harbored a significant electrocatalytic activity with a detection limit of 0.8 nM for BPA and 1.7 nM for BPS (S/N = 3). Correspondingly, the electrochemical response current was linearly correlated to BPA and BPS, ranging from 0.01 to 100 μM. Fe-HHTP/PGE also obtained satisfactory recoveries by 93.8–102.1% and 96.0–101.3% for detecting BPA and BPS in plastic food packaging samples. Our work has provided a novel electrochemical tool to simultaneously detect BPA and BPS in food packaging samples and environmental matrixes.

Background: In the plastics production sector, bisphenol S (BPS) has gained popularity as a replacement for bisphenol A (BPA). However, the mode of action (MOA) of female reproductive toxicity caused by BPS remains unclear and the safety of BPS is controversial. Methods: Human normal ovarian epithelial cell line, IOSE80, were exposed to BPS at human-relevant levels for short-term exposure at 24 h or 48 h, or for long-term exposure at 28 days, either alone or together with five signaling pathway inhibitors: ICI 18,2780 (estrogen receptor [ER] antagonist), G15 (GPR30 specific inhibitor), U0126 (extracellular regulated protein kinase [ERK] 1/2 inhibitor), SP600125 (c-Jun N-terminal kinase [JNK] inhibitor) or SB203580 (p38 mitogen‑activated protein kinase [p38MAPK] inhibitor). MOA through ERβ-MAPK signaling pathway interruption was explored, and potential thresholds were estimated by the benchmark dose method. Results: For short-term exposure, BPS exposure at human-relevant levels elevated the ESR2 and MAPK8 mRNA levels, along with the percentage of the G0/G1 phase. For long-term exposure, BPS raised the MAPK1 and EGFR mRNA levels, the ERβ, p-ERK, and p-JNK protein levels, and the percentage of the G0/G1 phase, which was partly suppressed by U0126. The benchmark dose lower confidence limit (BMDL) of the percentage of the S phase after 24 h exposure was the lowest among all the BMDLs of a good fit, with BMDL5 of 9.55 μM. Conclusions: The MOA of female reproductive toxicity caused by BPS at human-relevant levels might involve: molecular initiating event (MIE)-BPS binding to ERβ receptor, key event (KE)1-the interrupted expression of GnRH, KE2-the activation of JNK (for short-term exposure) and ERK pathway (for long-term exposure), KE3-cell cycle arrest (the increased percentage of the G0/G1 phase), and KE4-interruption of cell proliferation (only for short-term exposure). The BMDL of the percentage of the S phase after 24 h exposure was the lowest among all the BMDLs of a good fit, with BMDL5 of 9.55 μM.

Bisphenols are endocrine-disrupting chemicals used in plastics and resins for food packaging. This study aimed to evaluate the exposure to bisphenol A (BPA), bisphenol S (BPS), and bisphenol F (BPF) associated with the consumption of fresh, canned, and ready-to-eat meals and determine the effects of bisphenols on blood pressure and heart rate. Forty-eight healthy young adults were recruited for this study, and they were divided into the following three groups: fresh, canned, and ready-to-eat meal groups. Urine samples were collected 2, 4, and 6 h after meal consumption, and blood pressure and heart rate were measured. The consumption of ready-to-eat meals significantly increased urine BPA concentrations compared with canned and fresh meal consumption. No significant difference in BPS and BPF concentrations was observed between the groups. The consumption of ready-to-eat meals was associated with a significant increase in systolic blood pressure and pulse pressure and a marked decrease in diastolic blood pressure and heart rate. No significant differences were noted in blood pressure and heart rate with canned and fresh meal consumption. It can be concluded that total BPA concentration in consumed ready-to-eat meals is high. High BPA intake causes increase in urinary BPA concentrations, which may, in turn, lead to changes in some cardiovascular parameters.

Bisphenols are dangerous endocrine disruptors that pollute the environment. Due to their chemical properties, they are globally used to produce plastics. Structural similarities to oestrogen allow bisphenols to bind to oestrogen receptors and affect internal body systems. Most commonly used in the plastic industry is bisphenol A (BPA), which also has negative effects on the nervous, immune, endocrine, and cardiovascular systems. A popular analogue of BPA-bisphenol S (BPS) also seems to have harmful effects similar to BPA on living organisms. Therefore, with the use of double immunofluorescence labelling, this study aimed to compare the effect of BPA and BPS on the enteric nervous system (ENS) in mouse jejunum. The study showed that both studied toxins impact the number of nerve cells immunoreactive to substance P (SP), galanin (GAL), vasoactive intestinal polypeptide (VIP), the neuronal isoform of nitric oxide synthase (nNOS), and vesicular acetylcholine transporter (VAChT). The observed changes were similar in the case of both tested bisphenols. However, the influence of BPA showed stronger changes in neurochemical coding. The results also showed that long-term exposure to BPS significantly affects the ENS.

The degradation of recalcitrant organic pollutants by sulphate radical (SO4•−) represents one of the most recent developments in oxidation-based water treatment. In most cases, persulfate (PS) acts as a precursor of sulphate radicals. This study employed ultrasound-activated PS to generate reactive species, facilitating the degradation of bisphenol S (BPS), a well-known contaminant of emerging concern (CECs). An ultrasound with a frequency of 620 kHz and 80 W power was utilised for the degradation studies. The applied oxidation system successfully resulted in the complete degradation of BPS in both pure and real environmental water samples. Additionally, the Chemical oxygen demand (COD) was reduced to an acceptable limit in both matrices, with a reduction of 85 % in pure water and 73 % in river water. The degradation was monitored by varying chemical parameters such as pH, inorganic ions, and organics concentration. The results indicate that under specific pH conditions, the degradation efficiency followed the order of pH 3 > 4 > 7 > 11. The presence of coexisting matrices suppressed the efficiency by scavenging the reactive species. Utilizing high-resolution mass spectrometry (HRMS) analysis, this study identified seven intermediate products during identified during the degradation of BPS. Furthermore, a comprehensive mechanism has been deduced for the transformation and degradation process. All the results presented in this study underscore the applicability of the US/PS system in the removal of CECs.

Bisphenol S (BPS) is a raw material that is used extensively in various manufacturing processes but possesses a high detection rate in human red blood cells (RBCs). Accordingly, BPS is a potential toxicant in disturbing the function of RBCs and causing RBC-related diseases. To date, the effects and mechanisms of BPS-induced RBC-related diseases have not been elucidated. Here, using different models, including rats, zebrafish embryos and RBCs, the underlying mechanism of RBC-related diseases induced by BPS was explored. The accumulation of BPS in tissue was colon > kidney > liver > plasma > testicle > heart > brain in SD rats orally administered BPS (10 and 50 mg/kg bw/day) for 32 days, which was similar in both 10 mg/kg bw/day and 50 mg/kg bw/day group. Rats given BPS orally developed hyperlipidemia and increased RBC membrane cholesterol, as well as changes in RBC morphology and function. Moreover, BPS at the concentrations measured in rats plasma caused oxidative stress and phosphatidylserine exposure in vitro RBCs. These combined factors led to RBC aggregation in blood and an increasing in the number of RBCs in the blood vessels of the liver in rats. The dynamic visual observation of RBCs in vein vessels of zebrafish embryos exposed to BPS at 0, 1, 10 and 100 μg/L further found that the flow of RBCs in the tail vein is slow or even immobile, posing the risk of venous thrombosis. The present study provides new insight into the links between environmental pollutants and venous thrombosis.

Pregnancy and lactation are critical periods for human well-being and are sensitive windows for pollutant exposure. Bisphenol A (BPA) is well demonstrated as a toxicant and has been replaced in the plastic industry with other bisphenol analogs that share similarities in structure and characteristics, most commonly Bisphenol S (BPS) and Bisphenol F (BPF). Maternal exposure to BPS or BPF can result in their accumulation in the fetal compartment, leading to chronic exposure and potentially limiting normal fetal growth and development. This review summarizes considerable findings of epidemiological or experimental studies reporting associations between BPS or BPF and impaired fetal growth and development. Briefly, the available findings indicate that exposure to the two bisphenol analogs during pregnancy and lactation can result in multiple disturbances in the offspring, including fetal growth restrictions, neurological dysfunctions, and metabolic disorders with the potential to persist throughout childhood. The occurrence of premature births may also be attributed to exposure to the two bisphenols. The possible mechanisms of actions by which the two bisphenols can induce such effects can be attributed to a complex of interactions between the physiological mechanisms, including impaired placental functioning and development, dysregulation of gene expression, altered hormonal balance, and disturbances in immune responses as well as induced inflammations and oxidative stress. In conclusion, the available evidence suggests that BPS and BPF have a toxic potential in a compartment level to BPA. Future research is needed to provide more intensive information; long-term studies and epidemiological research, including a wide scale of populations with different settings, are recommended. Public awareness regarding the safety of BPA-free products should also be enhanced, with particular emphasis on educating individuals responsible for the well-being of children. [ABSTRACT FROM AUTHOR]

The article evaluates bisphenol release from different clear aligner materials using liquid chromatography-mass spectrometry/mass spectrometry. Topics include the types of bisphenols analyzed (Bisphenol A, Bisphenol F, Bisphenol S), the comparison of release among clear aligner brands, and the significance of the findings under the study conditions.

Negative public sentiment built up around bisphenol A (BPA) follows growing awareness of the frequency of this chemical compound in the environment. The increase in air, water, and soil contamination by BPA has also generated the need to replace it with less toxic analogs, such as Bisphenol F (BPF) and Bisphenol S (BPS). However, due to the structural similarity of BPF and BPS to BPA, questions arise about the safety of their usage. The toxicity of BPA, BPF, and BPS towards humans and animals has been fairly well understood. The biodegradability potential of microorganisms towards each of these bisphenols is also widely recognized. However, the scale of their inhibitory pressure on soil microbiomes and soil enzyme activity has not been estimated. These parameters are extremely important in determining soil health, which in turn also influences plant growth and development. Therefore, in this manuscript, knowledge has been expanded and systematized regarding the differences in toxicity between BPA and its two analogs. In the context of the synthetic characterization of the effects of bisphenol permeation into the environment, the toxic impact of BPA, BPF, and BPS on the microbiological and biochemical parameters of soils was traced. The response of cultivated plants to their influence was also analyzed. [ABSTRACT FROM AUTHOR]

Bisphenol S (BPS) is a novel bisphenol A (BPA) analogue, a ubiquitous environmental pollutant that disrupts male reproductive system. Whether BPS affects Leydig cell maturation in male puberty remains unclear. Male Sprague–Dawley rats (age of 35 days) were daily gavaged to 0, 1, 10, 100, and 200 mg/kg/day from postnatal days 35–56. BPS at 1–10 mg/kg/day and higher doses markedly reduced serum testosterone and progesterone levels but it at 200 mg/kg/day significantly increased estradiol level. BPS at 100 and 200 mg/kg/day significantly elevated serum luteinizing hormone (LH) levels. BPS at 1–10 mg/kg/day and higher doses significantly reduced inhibin A and inhibin B levels. BPS at 100 and 200 mg/kg/day markedly increased CYP11A1+ Leydig cell number, but did not affect HSD11B1+ (a mature Leydig cell marker) cell number. BPS at 10 mg/kg/day and higher doses significantly downregulated the expression of Cyp11a1 and at 100 and 200 mg/kg/d significantly lowered Cyp17a1, Hsd11b1, and Nr5a1 in the testes. BPS at 100 and/or 200 mg/kg/day significantly elevated Lhb in the pituitary. BPS at 100 and 200 mg/kg/day significantly increased the phosphorylation of AKT1, AKT2, and CREB without affecting total AKT1, AKT2, and CREB levels. BPS at 1–100 μM significantly suppressed testosterone production and induced proliferation of primary immature Leydig cells after 24 h of treatment and these actions were reversed by estrogen receptor α antagonist, ICI 182780, and partially reversed by vitamin E. BPS at 0.1–10 μM significantly increased oxidative stress of Leydig cells in vitro. BPS also directly inhibited 17β‐hydroxysteroid dehydrogenase 3 activity at 10–100 μM. In conclusion, BPS causes hypergonadotropic androgen deficiency in male rats during pubertal exposure via activating ESR1 and inducing ROS in immature Leydig cells and directly inhibiting 17β‐hydroxysteroid dehydrogenase 3 activity. [ABSTRACT FROM AUTHOR]

Introduction: Bisphenol A (BPA) is used in large quantities for the production of plastics and is present in various everyday objects. It penetrates living organisms and shows multidirectional adverse influence on many internal organs. For this reason, BPA is often replaced in plastic production by other substances. One of them is bisphenol S (BPS), whose effects on the enteric nervous system (ENS) have not been explained. Methods: Therefore, the present study compares the influence of BPA and BPS on the number of enteric neurons immunoreactive to cocaine-and amphetamine-regulated transcript (CART) peptide located in the ENS of the stomach, jejunum and colon with the use of double immunofluorescence method. Results: The obtained results have shown that both bisphenols studied induced an increase in the number of CART-positive enteric neurons, and the severity of changes depended on the type of enteric ganglion, the dose of bisphenols and the segment of the digestive tract. The most visible changes were noted in the myenteric ganglia in the colon. Moreover, in the colon, the changes submitted by BPS are more noticeable than those observed after BPA administration. In the stomach and jejunum, bisphenol-induced changes were less visible, and changes caused by BPS were similar or less pronounced than those noted under the impact of BPA, depending on the segment of the gastrointestinal tract and ganglion type studied. Discussion: The results show that BPS affects the enteric neurons containing CART in a similar way to BPA, and the BPS impact is even stronger in the colon. Therefore, BPS is not neutral for the gastrointestinal tract and ENS. [ABSTRACT FROM AUTHOR]

Bisphenol F (BPF) and bisphenol S (BPS) have become popular substitutes for bisphenol A (BPA) in the plastic industry due to concerns over BPA's adverse effects. However, there is limited information on children's exposure to these chemicals. This study aims to assess the extent of BPA, BPF, and BPS exposure and determine factors that influence such exposure. A group of Thai children (age 6–13 years, N = 358) were recruited between October 2019 and 2020. Two first-morning voids were collected one week apart. Demographic and exposure-related information was gathered. Urinary concentrations of bisphenols were analyzed by liquid chromatography and tandem mass spectrometry. Correlation between bisphenol concentrations with age, body weight, and sources of bisphenol exposure, was determined using generalized estimating equations with linear model. BPA, BPF, and BPS were detected at 79.6%, 31.0%, and 16.8%, with geometric mean (GM) concentrations of 1.41, 0.013, and 0.014 ng/mL, respectively. Younger children aged <10 years exhibited 1.3–1.6 times higher GM levels of all bisphenols compared to older children. Exposure to food stored in plastic containers was associated with higher levels of BPF and BPS. In conclusion, BPA was the most frequently detected bisphenol in urine samples from Thai children, followed by BPF and BPS. [ABSTRACT FROM AUTHOR]

Bisphenol S (BPS) is an environmental pollutant that can accumulate in the human body and cause harm. Puerarin (PUE) is a flavonoid with anti-inflammatory and antioxidant effects. In this study, we used 50 mg/kg/d BPS as a poison and PUE as an intervention for model mice for 42 d. BPS exposure significantly increased the levels of the impairment of the mice's liver function, T-CHO, TG, LDL-C, ALT, and AST in the BPS group were significantly increased (p < 0.05). Additionally, BPS exposure caused inflammatory cell infiltration in the mice liver tissue and enhanced oxidative stress response, the level of MDA was significantly increased (p < 0.05). The expression of CD36 and pparγ was stimulated after BPS exposure. Moreover, the expression of cpt1a and cpt1b, which promote fatty acid oxidation, was downregulated. After PUE intervention, the levels of genes and proteins involved in lipid synthesis (PPARγ, SREBP1C, and FASN) and metabolism (Cpt1a, Cpt1b, and PPARα) in mice returned to those of the control group, or much higher than those in the BPS group. Therefore, we hypothesized that BPS causes lipid accumulation in the liver by promoting lipid synthesis and reducing lipid metabolism, whereas PUE reduces lipid synthesis and promotes lipid metabolism. Conclusively, our results imply that long-term exposure to BPS in mice affects liver lipid metabolism and that PUE intervention could maintain the liver function of mice at normal metabolic levels. [ABSTRACT FROM AUTHOR]

The photoreceptor necessitates the retinoids metabolism processes in visual cycle pathway to regenerate visual pigments and sustain vision. Bisphenol S (BPS), with similar structure of thyroid hormone (TH), was reported to impair the light-sensing function of zebrafish larvae via disturbing TH-thyroid hormone receptor β (TRβ) signaling pathway. However, it remains unknown whether TRβ could modulate the toxicity of BPS on retinoid metabolism in visual cycle. This study showed that BPS diminished the optokinetic response of zebrafish larvae and had a stimulative effect on all-trans-retinoic acid (atRA) metabolism, like exogenous T3 exposure. By modulating CYP26A1 and TRβ expression, it was found that CYP26A1 played a crucial role in catalyzing oxidative metabolism of atRA and retinoids regeneration in visual cycle, and TRβ mediated cyp26a1 expression in zebrafish eyes. Similar with 10 nM T3 treatment, cyp26a1 expression could be induced by BPS in the presence of TRβ. Further, in CYP26A1 and TRβ- deficient eyes, 100 μg/L BPS could no longer promote atRA metabolism, or decrease the all-trans-retinol and 11-cis retinal contents in visual cycle, demonstrating that BPS exposure disturbed CYP26A1-mediated visual retinoids metabolism via TRβ. Overall, this study highlights the role of TRβ in mediating the retinoids homeostasis disruption caused by BPS, and provides new clues for exploring molecular targets of visual toxicity under pollutants stress.

Ever‐increasing occurrence of plastic‐manufacturing industries leads to environmental pollution that has been associated with declined human health and increased incidence of compromised reproductive health. Female subfertility/infertility is a complex phenomenon and environmental toxicants as well as lifestyle factors have a crucial role to play. Bisphenol S (BPS) was believed to be a "safer" replacement of bisphenol A (BPA) but recent data documented its neurotoxic, hepatotoxic, nephrotoxic, and reprotoxic attributes. Hence based on the scarcity of reports, we investigated molecular insights into BPS‐induced ovarian dysfunction and protective actions of melatonin against it in adult golden hamsters, Mesocricetus auratus. Hamsters were administered with melatonin (3 mg/kg BW i.p. alternate days) and BPS (150 mg/kg BW orally every day) for 28 days. BPS treatment disrupted hypothalamo–pituitary–ovarian (HPO) axis as evident by reduced gonadotropins such as luteinizing hormone (LH) and follicle‐stimulating hormone (FSH), ovarian steroids such as estradiol (E2) and progesterone (P4), thyroid hormones namely triiodothyronine (T3) and thyroxine (T4) and melatonin levels along with their respective receptors (ERα, TRα, and MT‐1) thereby reducing ovarian folliculogenesis. BPS exposure also led to ovarian oxidative stress/inflammation by increasing reactive oxygen species and metabolic disturbances. However, melatonin supplementation to BPS restored ovarian folliculogenesis/steroidogenesis as indicated by increased number of growing follicles/corpora lutea and E2/P4 levels. Further, melatonin also stimulated key redox/survival markers such as silent information regulator of transcript‐1 (SIRT‐1), forkhead box O‐1 (FOXO‐1), nuclear factor E2‐related factor‐2 (Nrf2), and phosphoinositide 3‐kinase/protein kinase B (PI3K/pAkt) expressions along with enhanced ovarian antioxidant capacity. Moreover, melatonin treatment reduced inflammatory load including ovarian nuclear factor kappa‐B (NFĸB), cyclooxygenase‐2 (COX‐2), and inducible nitric oxide synthase (iNOS) expressions, serum tumor necrosis factor α (TNFα), C‐reactive protein (CRP) and nitrite–nitrate levels as well as upregulated ovarian insulin receptor (IR), glucose uptake transporter‐4 (GLUT‐4), connexin‐43, and proliferating cell nuclear antigen (PCNA) expressions in ovary thereby ameliorating inflammatory and metabolic alterations due to BPS. In conclusion, we found severe deleterious impact of BPS on ovary while melatonin treatment protected ovarian physiology from these detrimental changes suggesting it to be a potential preemptive candidate against environmental toxicant‐compromised female reproductive health. [ABSTRACT FROM AUTHOR]

Fenton-like oxidation processes are widely used to degrade recalcitrant organic pollutants, but are limited by narrow application pH and low reaction efficiency. This study investigated the synchronous activation of H2O2 and persulfate (PDS) by sulfidated zero valent iron (S-nZVI) in ambient conditions for Fenton-like oxidation of bisphenol S (BPS), an estrogenic endocrine-disrupting chemical. The activation of S-nZVI induced H2O2 or PDS could be greatly enhanced with the assistance of PDS and H2O2, respectively, even across a wide range of pH value (3–11). The first-order rate constant of S-nZVI/H2O2/PDS, S-nZVI/PDS and S-nZVI/H2O2 systems was found to be 0.2766 min−1, 0.0436 min−1, and 0.0113 min−1, respectively. A significant synergy between H2O2 and PDS was achieved when the PDS-H2O2 molar ratio was above 1:1, and where sulfidation promoted iron corrosion and decreased solution pH were observed in the S-nZVI/H2O2/PDS system. Radical scavenging experiments and electron paramagnetic resonance (EPR) investigations suggest that both SO4•− and •OH were generated and that •OH played a crucial role in BPS removal. Furthermore, four BPS degradation intermediates were detected and three degradation pathways were proposed in line with the HPLC-Q-TOF–MS analysis. This study demonstrated that compared to the traditional Fenton-like system, the S-nZVI/H2O2/PDS system could be a more efficient, advanced oxidation technology capable of being used across a broad pH range for emerging pollutants' degradation. [ABSTRACT FROM AUTHOR]

Bisphenol A (BPA) analogs, like BPA, could have adverse effects on human health including bone health. The aim was to determine the effect of BPF, BPS and BPAF on the growth and differentiation of cultured human osteoblasts. Osteoblasts primary culture from bone chips harvested during routine dental work and treated with BPF, BPS, or BPAF for 24 h at doses of 10–5, 10–6, and 10–7 M. Next, cell proliferation was studied, apoptosis induction, and alkaline phosphatase (ALP) activity. In addition, mineralization was evaluated at 7, 14, and 21 days of cell culture in an osteogenic medium supplemented with BP analog at the studied doses. BPS treatment inhibited proliferation in a dose-dependent manner at all three doses by inducing apoptosis; BPF exerted a significant inhibitory effect on cell proliferation at the highest dose alone by an increase of apoptosis; while BPAF had no effect on proliferation or cell viability. Cell differentiation was adversely affected by treatment with BPA analogs in a dose-dependent, observing a reduction in calcium nodule formation at 21 days. According to the results obtained, these BPA analogs could potentially pose a threat to bone health, depending on their concentration in the organism. [ABSTRACT FROM AUTHOR]

Background: Bisphenol A (BPA) and its alternatives (BPF, BPS) are widely used in daily consumer products, which commonly expose humans to these chemicals. Bisphenols (BPs) are endocrine-disrupting chemicals widely present in the environment and can accumulate in the entire food chain by circulating in the ecosystem. In humans, BPs intake leads to accumulation in the human body and causes many chronic diseases, including endocrine disruption, immunotoxicity, and cancer. Objective: Although several studies have demonstrated the negative effect of BPA and its alternatives, studies have yet to be determined whether bisphenols can affect human trophoblast cells. Thus, this study aimed to analyze the toxic effect of BPs on the human trophoblast cell line BeWo. Results: We investigated the cytotoxic effect of BPs on human trophoblast cells. The cytotoxicity was measured by the MTS assay and flow cytometric analysis that representing the cell viability, cell proliferation, cell cycle progression and apoptotic cell death. BPs had no effect on BeWo cell viability at concentrations below 100 mM, and did not cause significant changes in cell proliferation and apoptosis. However, BPA and BPS altered cell cycle progression and checkpoint regulator expression. Conclusion: BPs did not affect cell viability and proliferation. However, BPS altered the G0/G1 and G2/M phases of the trophoblast BeWo cells by increasing cyclin B1 expression. [ABSTRACT FROM AUTHOR]

This study investigated whether the coadministration of vitamin E (VitE) diminishes the harmful effects provoked by plasticizer bisphenol S (BPS) in the serum metabolites related to hepatic and renal metabolism, as well as the endocrine pancreatic function in diabetic male Wistar rats. Rats were divided into five groups (n = 5–6); the first group was healthy rats (Ctrl group). The other four groups were diabetic rats induced with 45 mg/kg bw of streptozotocin: Ctrl-D (diabetic control); VitE-D (100 mg/kg bw/d of VitE); BPS-D (100 mg/kg bw/d of BPS); The animals from the VitE + BPS-D group were administered 100 mg/kg bw/d of VitE + 100 mg/kg bw/d of BPS. All compounds were administered orally for 30 days. Body weight, biochemical assays, urinalysis, glucose tolerance test, pancreas histopathology, proximate chemical analysis in feces, and the activity of antioxidants in rat serum were assessed. The coadministration of VitE + BPS produced weight losses, increases in 14 serum analytes, and degeneration in the pancreas. Therefore, the VitE + BPS coadministration did not have a protective effect versus the harmful impact of BPS or the diabetic metabolic state; on the contrary, it partially aggravated the damage produced by the BPS. VitE is likely to have an additive effect on the toxicity of BPS. [ABSTRACT FROM AUTHOR]

Bisphenol S (BPS), an organic compound and bisphenol analog, is commonly used as a substitute for bisphenol A. BPS is widely used in epoxy glues, can coatings, and thermal receipt papers; however, its risks have not been fully determined and the probability of its toxicity has been continuously suggested. In this study, we conducted BPS toxicity tests on aquatic plants (acute), cladocerans (acute and chronic), and fish (chronic) to determine its adverse effects, and calculated the toxicity values. Additionally, we conducted an ecological risk assessment of BPS in freshwater ecosystems with toxicity data from previous studies using the species sensitivity distribution method and BPS exposure data from 14 rivers in four countries in Asia (China, Japan, India, and South Korea). The chronic-based risk quotient (RQ) values of BPS in one river in China and two rivers in India were > 1, indicating a high ecological risk of BPS to aquatic organisms. The other four rivers in China showed medium ecological risk (0.1 < RQ < 1) and those in Japan and South Korea showed negligible chronic risk (RQ < 0.1) to aquatic organisms. We also suggest sensitive indicators in the model organism Danio rerio and highlighted the importance of the development of new method of ecological risk assessment. This study could provide new information that will assist in managing BPS and bisphenol analogs in freshwater ecosystems. [ABSTRACT FROM AUTHOR]

Bisphenol A (BPA) substitutes, such as bisphenol S (BPS) and bisphenol AF (BPAF), are increasingly used due to restrictions on BPA usage, a known endocrine disrupting chemical and putative obesogen. However, little is known about the obesogenic effects of exposure to BPA substitutes in children. A total of 426 children aged 7 years old originally recruited from Laizhou Wan Birth Cohort in Shandong, China, during 2010–2013 participated in the 2019–2020 survey. Urinary BPA and its substitutes including BPS, BPAF, bisphenol B (BPB), bisphenol AP (BPAP), bisphenol Z (BPZ), and bisphenol P (BPP) were determined. Anthropometric measures including height, weight, waist circumference, and body fat percentage were assessed, and overweight/obesity was defined as BMI z-score ≥ 85th percentile. Linear and logistic regressions were used on continuous and binary obesity measures, respectively, and weighted quantile sum (WQS) regression was further used to estimate the mixture effects of exposure to diverse bisphenols, and sex-stratified analysis was performed. BPA substitutes were widely detected (> 75%) in children's urine samples. A positive association with obesity measures was consistently observed for urinary BPS and BPAF, i.e., BMI z-score, waist circumference, and overweight/obesity. Further analysis from the WQS regression model demonstrated a positive association between bisphenol mixtures and all measures of obesity, with BPAF contributing the greatest weighing to the observed associations. Sex difference might exist as the positive associations were only significant in boys. No significant association was found between obesity and BPA or other BPA substitutes. Our study adds to mounting evidence that BPA substitutes BPS and BPAF are linked to obesity in children, especially in boys. Further longitudinal studies with larger sample size with continued biomonitoring these chemicals and their obesogenic effects are necessary. [ABSTRACT FROM AUTHOR]

In this study, peanut shell was modified using ß-cyclodextrin (ß-CD) and citric acid to improve the adsorption capacity for removal of lead ion (Pb2+) and bisphenol S (BPS) from solution in batch mode. Scanning electron microscopy, Fourier-transform infrared spectroscopy, elemental analysis, X-ray fluorescence analysis, specific surface area analysis, thermogravimetric analysis, etc were used to characterize the adsorbent before and after modification. The results showed that the adsorbent was successfully modified. The adsorption results of Pb2+ and BPS on ß-CD-PS indicated that acidic conditions were not conducive to the adsorption of Pb2+, the adsorption of BPS basically remained unchanged at pH 2~7, and alkaline conditions were not conducive to the adsorption. The presence of salt had a negative effect on Pb2+, but had no effect on the adsorption of BPS. The Langmuir and Koble-Corrigan models could predict the equilibrium adsorption process of Pb2+ while Temkin and Koble-Corrigan models could describe the equilibrium adsorption process of BPS. The adsorption quantity from experiments is 89.6 mg·g-1 for Pb2+ and 16.2 mg·g-1 for BPS at 293 K, respectively. The adsorption process of Pb2+ was consistent with the pseudo-first-order and Elovich models, indicating the presence of ion-exchange in the adsorption process; the adsorption of BPS was consistent with the pseudo-second-order model, indicating that chemisorption was the main rate-controlling step. Thermodynamic studies indicated that the adsorption of Pb2+ was a spontaneous and endothermic reaction with increasing entropy, while the adsorption of BPS was a spontaneous and exothermic reaction with decreasing entropy. 0.1 mol·L-1 HNO3 could desorb and regenerate the ß-CD-PS adsorbed Pb2+ for three times, and 75% C2H5OH had a better desorption and regeneration effect for BPS loaded ß-CD-PS. ß-CD-PS can effectively remove the lead ion and BPS from mixtures and the study can provide the basis for the effective utilization of peanut shell in environmental remediation. [ABSTRACT FROM AUTHOR]

Caenorhabditis elegans represents a favorite non-mammalian animal model, which is often used to study the effect of foreign substances on living organisms. Its epidermal barrier is a primary biological barrier that protects nematodes from the toxicity of chemicals. In this study, we investigated the effect of Bisphenol A (BPA), an endocrine disrupting chemical, and its structural analog Bisphenol S (BPS), which is often used as a substitute for BPA in some products, on the behavior of C. elegans wild type (N2) and C. elegans bli-1 mutant strain, which is characterized by the production of abnormal cuticle blisters. We found that exposure of C. elegans wild type (N2), as well as its mutant strain bli-1, to selected concentrations of BPA (0.1, 0.5, 1 and 5 µM) and BPS (0.1, 0.5, 1 and 5 µM) resulted in significant changes in reproduction, habituation behavior, and body length of nematodes. Based on our findings, we can conclude that BPS, which was supposed to be a safer alternative to BPA, caused almost identical detrimental effects on C. elegans behavior. Furthermore, compared to the wild type of C. elegans, these effects were more pronounced in the bli-1 strain, which is characterized by a mutation in an individual collagen gene responsible for proper cuticle formation, underlying the role of the epidermal barrier in bisphenol toxicity. Taken together, our data indicate the potential risks of using BPS as a BPA alternative.

Abstract Background Bisphenol A (BPA) exposure and its structural analogs (BPS and BPF) might cause endocrine alterations and adverse physiological effects. Few studies to date have directly explored the association between its structural analogs (BPS, BPF) and sex hormones in adult male participants. Therefore, we aimed to assess the associations between BPA, BPS, BPF, and sex hormones in American adult men. Methods We used data from the U.S. National Health and Nutrition Examination Survey 2011–2016. We excluded participants without data available on sex hormones and urinary bisphenols. Furthermore, participants consuming sex hormone medications were excluded. Multivariable regression models were performed to assess the association between bisphenols and sex hormones. Results In this study, 2367 participants were included. Of 2367, in 1575 participants, the data on BPS and BPF were available. We found that a per unit increase in BPF was associated with 0.575 ng/dL higher total testosterone (TT) (Model 2: 95% CI: 0.047, 1.103, P = 0.033). However, there was no significant association between BPA or BPS and TT. Furthermore, increased BPA and BPS levels were associated with higher levels of sex hormone-binding globulin (SHBG) (Model 2: β = 0.364, 95% CI: 0.158, 0.571; β = 0.25, 95% CI: 0.071, 0.429, respectively). Additionally, participants in the highest BPA exposure quartile (quartile 4) had 4.072 nmol/L higher levels of SHBG than those in quartile 1 (Model 2: 95% CI: 0.746, 7.397, P = 0.017; P for trend =0.005). Both BPA and BPS were negatively associated with free testosterone (FT, nmol/L) after full adjustment (Model 2, β = − 0.01%, P = 0.0211, P = 0.0211; Model 2, β = − 0.01%, P = 0.0258, respectively). However, BPF was positively associated with FT (Model 2, β = 0.0029%, P = 0.0028). Conclusion Our study indicated that exposure to both BPA and its substitutions could alter sex hormone levels. This finding supports the possibility that human exposure to bisphenols at environmental levels might affect the endogenous hormone balance.

There is considerable evidence that Bisphenol S (BPS) induces various toxicological effects and is an industrial health issue. However, little data are available on the in vivo effects of BPS on the liver, a major target of drug toxicity. In this study, we evaluated the potential harmfulness of low levels of BPS in the liver of male mice. Also, we investigated the interaction between BPS and peroxisome proliferator-activated receptor-gamma (PPARγ) by computational docking approach. PPARγ is a member of the superfamily of nuclear hormone receptors. It acts as a transcription factor and regulates the genes involved in lipid and glucose metabolism and in inflammation and necrosis. Mice were exposed to BPS, in drinking water at 25, 50, and 100 μg/kg for 10 weeks. The protocol was started after weaning. At the time of sacrifice, blood samples were collected for a biochemical analysis, followed by liver tissue collection for histopathological study. Results showed that BPS-induced hypertriglyceridemia, increased liver injury markers, and initiated histopathological changes, including inflammatory cell infiltration, hepatocellular necrosis, and steatosis. BPS did not affect glycated hemoglobin (HbA1C). Interestingly, data showed that BPS could interact with the PPARγ ligand-binding pocket by hydrogen bonds with Asn 219, Cys 276, Ser 280, and Thr 283. We suggest that PPARγ is among the targets of BPS and could play a key role in the cascade reaction of BPS-induced liver disruption. These findings support the hypothesis that the post-weaning period is sensitive to low-dose BPS exposure that can lead to dyslipidemia signature later in life. [ABSTRACT FROM AUTHOR]

Environmental estrogens (EEs) are associated with an increased prevalence of asthma. These epigenetic alterations of the immune cells may explain the multigenerational effects on asthma development. We hypothesized that exposure to immune cells enhances allergic sensitization by initiating signaling in these cells. Human T cell lines (TIB-152, CCL-119) were exposed to varying concentrations of estradiol, bisphenol A, bisphenol S, or bisphenol A + estradiol. H3K27me3, phosphorylations of EZH2 (pEZH2), AKT (pAKT), and phosphatidylinositide 3-kinase (pPI3K) were assessed. pAKT and pPI3K were decreased in response to some of the concentrations of these exposures in both cell lines. It is likely that EEs exposure to immune cells is one of the factors in the increase in the prevalence of asthma. • We observed the altered pAKT/pPI3K, pEZH2, and H3K27me3 in human T cells in response to endogenous and exogenous estrogens. • The pathway of rapid estrogen receptor signaling on these cells is likely different from reproductive cells. • It is likely that estrogen exposure to immune cells is one of the factors in the increase in the prevalence of asthma. [ABSTRACT FROM AUTHOR]