Search Results (55)

Bisphenol AF (BPAF), a prevalent bisphenol A (BPA) substitute, raises concerns due to its environmental persistence and endocrine-disrupting potency. While metabolic effects of direct exposure are documented, its intergenerational consequences remain unclear. Here, we demonstrated that perinatal BPAF exposure induced persistent metabolic syndrome in offspring, including glucose intolerance, hepatic steatosis, and adipose hypotrophy. Integrating multi-omics data, we observed that BPAF exposure shaped offspring’s hepatic epigenome, as demonstrated by genome-wide alterations in H3K27ac-marked regulatory elements. This epigenetic rewiring indicated a dual regulatory effect on transcriptomes that suppressed interferon-γ responses while activating sterol biosynthesis, ultimately perturbating hepatic metabolome, including depleted pantothenate levels and accumulation of pro-inflammatory eicosanoids. Our findings suggest that BPAF may act as a developmental toxicant capable of persistently disrupting the immune–metabolic axis through epigenomic mechanisms, highlighting the need for careful re-evaluation of its use as a BPA substitute in consumer products. Full article

Endocrine disruptors, including bisphenol A, S, AF, and F, have been demonstrated to exhibit endocrine-disrupting activity. This phenomenon has been associated with a variety of health problems, including (but not limited to) neurological and reproductive disorders. Given the potential hazards, it is essential to have effective tools to assess their toxicity. The nematode Caenorhabditis elegans has become a widely used model organism for studying bisphenols because of its genetic simplicity and the conservation of its fundamental biological processes. This review article summarizes current knowledge of bisphenol toxicity and the use of the model organism C. elegans as a high-throughput system for investigating the toxicological profiles of BPA and its emerging alternatives. Furthermore, we highlight the specific methodologies for assessing the toxic effects of bisphenols in C. elegans. While highlighting its advantages, we critically discuss its limitations, including the absence of specific metabolic organs, which constrain direct extrapolation to mammalian systems. Based on available evidence, we conclude that C. elegans serves as an essential bridge between in vitro assays and mammalian models, offering a powerful platform for the early hazard identification and mechanistic screening of bisphenol analogues. Full article

Bisphenol A (BPA), a synthetic industrial compound widely found in plastics and other materials, has been linked to cancer development. As human exposure increases, BPA may pose potential carcinogenic concerns. Although BPA binds to estrogen receptors with much lower affinity than natural estrogens, its accumulation in human tissues can cause harmful effects. This review summarizes current evidence on BPA’s role in cancer initiation and progression, with a focus on its effects on cancer signaling pathways. These effects involve modulating pathways involved in cell growth, movement, invasion, survival, and adhesion. BPA acts as an estrogen ligand, binding to estrogen receptors and activating related pathways. The main route of exposure is through dietary intake of canned and plastic-packaged foods, with migration rates increasing at higher temperatures. To raise awareness of BPA’s harmful effects, industries have proposed “BPA-free” alternatives, some of which use derivatives like bisphenol S (BPS) and bisphenol F (BPF), which, unfortunately, may have even worse effects on human health. Given the ongoing challenges of eliminating BPA and similar harmful compounds, future research should focus on identifying safe substitutes, developing more effective removal technologies, and strengthening stringent regulations to mitigate public health risks. Full article

Bisphenol A (BPA) and its analogues, such as bisphenol AF (BPAF), are widely used mainly in the plastic industry. These compounds can leach into the environment and negatively impact living organisms, including farm animals such as pigs. The aim of the study was to evaluate concentrations of BPA and BPAF in plasma and tissues of pigs after oral administration at a lower—20 µg (10 µg BPA + 10 µg BPAF)/kg body weight (b.w.)/day—and higher dose—60 µg (30 µg BPA + 30 µg BPAF)/kg b.w./day—for 21 days. The concentrations of BPA and BPAF in plasma and liver were monitored immediately after finishing the bisphenols administration, as well as two and four weeks after that. Generally, pigs receiving higher doses of BPA/BPAF showed the highest levels across most parameters, followed by those with lower doses and the control group. Results showed that both bisphenols remained in the organs of experimental pigs for two and four weeks after the administration was completed, respectively. Results also showed that the growth rate did not have a significant effect on the accumulation of bisphenols in pig tissues. The results of the present study have shown that oral administration of bisphenols led to an increase in the concentration of BPA and BPAF in plasma and other tissues of young pigs. Moreover, the fact that both BPA and BPAF were also detected in control pigs suggests that the farm environment was contaminated with these substances. This may pose a risk not only to the health and performance of pigs but also to human health, through the consumption of pig organs. Full article

Micro-nano bubbles (MNBs) have been widely used in water treatment due to their large specific surface area, long retention time, and high zeta potential. This study investigated the degradation of bisphenols by activating persulfate (PDS, an oxidizing agent) with air MNBs (MNBs/PDS). The removal rate of bisphenol A (BPA) in the MNBs/PDS process was 98.3% within 25 min, while there was almost no degradation observed by PDS or MNBs alone. This enhancement was attributed to the huge amount of energy released during the collapse of MNBs, sufficient to break the O–H bonds of water molecules or the O–O bond of PDS to induce the formation of reactive oxygen species (ROS, such as HO^• and SO₄^•−). To qualitatively analyze ROS generated in this system, electron paramagnetic resonance and quenching experiments were conducted, and the HO^• and SO₄^•− were detected in MNBs/PDS. Furthermore, the degradation percentages of bisphenols after 25 min of MNBs/PDS treatment followed the order of bisphenol B (100%) > BPA (98.3%) > bisphenol E (87.9%) > bisphenol F (86.5%) > bisphenol AF (84.9%) > bisphenol S (51%). Higher PDS dosage, higher gas flow rate, and lower pH values were preferred for the degradation. Moreover, the MNBs/PDS treatment reduced the TOC of secondary effluent containing BPA by 45.8% in one hour, indicating the application potential of MNBs/PDS in the advanced treatment of wastewater. Full article

Background/Objectives: Bisphenol AF (BPAF) is a prevalent environmental contaminant with demonstrated metabolic and immunological toxicity. This study aimed to investigate whether VDAC1 (Voltage-Dependent Anion Channel 1) mediates BPAF-induced succinate dysmetabolism and inflammatory responses in macrophages, and to evaluate the therapeutic potential of VDAC1 silencing. Methods: RAW264.7 macrophages were exposed to BPAF (0–2500 nM, 24 h) with or without VDAC1 siRNA transfection. Succinate levels, SDH activity, mitochondrial function (complexes I–V, ATP, membrane potential), and inflammatory markers (TNF-α, IL-6, IL-1β, ROS, MDA) were quantified. A 90-day oral toxicity study in C57BL/6J mice (0–32 mg kg⁻¹) assessed systemic inflammation and hepatic ultrastructure. p38 MAPK/NF-κB signaling was evaluated by Western blot and immunofluorescence. Results: BPAF elevated succinate 2.3-fold and decreased SDH activity by 48%, coinciding with reduced mitochondrial membrane potential and ATP synthesis (p < 0.01). Inflammatory cytokines and ROS were markedly increased. VDAC1 siRNA reversed these perturbations, restored complex II activity, and blunted p38 MAPK/NF-κB activation. In vivo, BPAF dose-dependently increased serum TNF-α, IL-6 and IL-1β, promoted NF-κB nuclear translocation and mitochondrial swelling, without altering body or liver weight; VDAC1 knockdown mitigated these effects. Conclusions: VDAC1 orchestrates BPAF-elicited succinate accumulation and macrophage inflammation via p38 MAPK/NF-κB signaling. Targeted VDAC1 silencing alleviates metabolic and inflammatory injury, offering a promising therapeutic strategy against BPAF-related diseases. Full article

Bisphenol (BP) compounds are widely present in the environment, primarily due to their use as plastic additives. These substances involve health risks, particularly as endocrine disruptors. While the general population is chronically exposed, patients with end-stage chronic kidney disease undergoing hemodialysis (HD-CKD) represent a particularly vulnerable group. This is due to both impaired renal clearance of circulating BPs and potential contamination from plastic-containing dialyzers used in extracorporeal blood circulation. In this longitudinal study, from the 35 HD-CKD patients initially selected, 25 changed their conventional dialyzers to BPA-free dialyzers for 6 months. Blood serum samples were collected, at baseline and after the intervention, to quantify levels of five BP analogues: Bisphenol A (BPA), Bisphenol AF (BPAF), Bisphenol F (BPF), Bisphenol B (BPB), and Bisphenol S (BPS). Genotoxicity was assessed using the comet assay and the micronucleus test on peripheral white blood cells. Among the analyzed BPs, only BPAF showed a statistically significant reduction when using BPA-free dialyzers. In terms of genotoxicity, a significant decrease was observed only in primary DNA damage (mainly DNA strand breaks), with no notable changes in chromosomal damage. This is the first study to detect multiple BP analogues in HD-CKD patients, beyond BPA, and to associate human exposure to BPs with DNA damage biomarkers. The observed reduction in DNA damage in parallel with decreased BPAF levels highlights the importance of monitoring and minimizing BP exposure of this high-risk population. Full article

Bisphenol AF (BPAF) exposure is increasingly linked to metabolic disorders, yet the molecular initiating events (MIE) and key events (KE) leading to hepatic steatosis remain unclear. We constructed an adverse outcome pathway (AOP) to mechanistically connect BPAF-triggered macrophage–hepatocyte crosstalk to liver fat accumulation. Male C57BL/6 mice received daily oral gavage of 0, 0.5, 4, or 32 mg kg⁻¹ BPAF for 90 d, and Transwell co-cultures of RAW264.7 macrophages and AML12 hepatocytes were used for in vitro validation. Targeted metabolomics, western blotting, and lipid staining quantified succinate, pathway proteins, and steatosis. BPAF dose-dependently increased serum succinate (BMD = 6901.95 nM) and hepatic triglyceride (TG) (BMD = 874.26 nM). Cryo-EM docking revealed BPAF binding to SUCNR1 at 2.9 Å, disrupting the inactive-state conformation. In co-culture, BPAF-exposed macrophages released succinate that bound hepatocyte SUCNR1, suppressed Akt phosphorylation, and activated JNK. These KEs led to a 40% increase in lipid droplets and elevated TG, total cholesterol (TC), and free fatty acids (FFA) without liver weight gain. We propose the first AOP for BPAF-induced hepatic steatosis: BPAF–SUCNR1 binding (MIE) → macrophage succinate release (KE1) → SUCNR1-mediated Akt inhibition/JNK activation (KE2–4) → hepatic lipid accumulation (KE5) → steatosis (AO). These findings provide mechanistic insight for chemical risk assessment of BPAF and structurally related bisphenols. Full article

Background: Bisphenols (BPs) are present in medical instruments, plastic containers, and personal care products (PCPs). Bisphenol A has been replaced by its alternatives, bisphenol S, F, AF, and B. Due to the awareness of their toxicity, mixed exposure to these alternatives at the regional level has been given less attention; there is a need to study this area of research. This meta-analysis examined the exposure of urinary bisphenol A and its metabolites to blood Hypothalamic–Pituitary–Thyroid axis hormones (HPT axis hormones) in pregnant women and adult males and females. We searched Embase, PubMed, Web of Science, Cochrane Library, and CINAHL until 8 January 2025, yielding 4588 articles using the PECO framework. Quality assessment was done using AHRQ: Agency for Healthcare Research and Quality for cross-sectional and NOS: Newcastle Ottawa Scale for cohort studies, with combined exposure evaluated using random and fixed-effect models. The I² test assessed heterogeneity. We included eighteen studies for the final analysis. Fixed-effect model estimates revealed that BPA is negatively associated with thyroid-stimulating hormone (TSH) in female and male adults (β = −0.02; 95% CI = −0.04 to −0.01); (β = −0.08; 95% CI = −0.14 to −0.02). In Females, BPA was positively associated with free thyroxine, FT4 (β = 0.001, 95% CI, 0.001 to 0.001). In the male group, BPA was negatively associated with FT4 (β = −0.001, 95% CI, −0.001 to −0.001). As per pregnant women, there was no association found between exposure to bisphenols and total Thyroxine (TT4), FT4, and TSH in both trimesters (β = 0.010, 95% CI = −0.030 to 0.050); (β = 0.001, 95% CI = −0.010 to 0.010); (β = −0.001, 95% CI = −0.010 to 0.001), respectively, for early pregnancy. Bisphenols can significantly influence HPT axis hormones in adult males, females, and pregnant women. Gender-based studies were observed, concluding that adult females are more affected by bisphenol exposures than adult males. The subgroup analysis based on the regions did not reveal any associations. Full article

BPAF (Bisphenol AF), one of the primary substitutes for BPA (Bisphenol A), is widely used in the production of plastics, optical fibers, and other materials. During the use of these products, BPAF inevitably enters the environment and exerts toxic effects on animal growth, development, reproduction, immunity, neurology, and genetics. This study employed marine medaka (Oryzias melastigma) as the experimental model to evaluate the toxicological impacts of BPAF on early development. Embryos were exposed to four BPAF concentrations (0, 1 μg/L, 10 μg/L, and 100 μg/L) for 14 days (embryonic to larval stages), followed by phenotypic measurements, behavioral analysis, and gene expression detection. The results demonstrated that BPAF exposure induced developmental malformations and reduced survival rates in marine medaka embryos, with embryo survival negatively correlated with BPAF concentrations. Additionally, BPAF significantly decreased embryonic heart rates, and the 100 μg/L BPAF group exhibited prolonged embryo hatching time and reduced hatching success. In newly hatched larvae, BPAF exposure led to decreased body length, reduced heart rates, and significant suppression of swimming activity, characterized by increased resting time and reduced swimming distance. BPAF exposure altered the expression levels of genes associated with cardiovascular function (e.g., tbx2b, arnt2), the HPT axis (e.g., tg, dio3a, trh, trhr2, tpo), and neurodevelopment (e.g., ache, elavl3, gfap) in the medaka larvae. These transcriptional perturbations are proposed as potential molecular mechanisms underlying the observed phenotypic effects, including reduced heart rates and suppressed swimming behavior in the study. Molecularly, BPAF exposure significantly disrupted the expression of genes related to the cardiovascular system, HPT axis, and nervous system. Full article

The growing use of plastics in food packaging has raised concerns about chemical migration into consumables, posing potential health risks. Ensuring the safety of packaging materials is a critical public health priority. This study aimed to validate an analytical method for qualitative and quantitative determination of BPs in bottled water and evaluate their presence in PET and rPET matrices. The method was validated through recovery tests for eight BPs (Bisphenol A, Bisphenol S, Bisphenol F, Bisphenol AF, Bisphenol AP, Bisphenol B, Bisphenol Z, and Bisphenol P). Linearity (R² ≥ 0.990) and high recovery rates proved the method’s stability, reliability, and accuracy. For bottled water, LODs ranged 0.030–0.075 µg/L and LOQs 0.10–0.25 µg/L; for PET/rPET, LODs were 0.00030–0.00075 mg/kg and LOQs 0.0010–0.0025 mg/kg. Mean recoveries in bottled water were in the range 89–109%, in PET from 94% to 117%, and in rPET from 106% to 118%. The results showed that BPA was quantifiable in all matrices, while other BPs remained below the limit of quantification. The validated method provides a robust tool for assessing bisphenol contamination and supports ongoing efforts to enhance food safety and inform regulatory frameworks for sustainable PET recycling. Full article

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

Bisphenol AF (BPAF) is widely utilized as an analog of bisphenol A (BPA) in the plastics industry. However, there is limited evidence on its neurodevelopmental toxicity. Existing studies suggest that BPAF has greater accumulation in vivo than other bisphenol analogs, and could pass through the placental barrier and the blood–brain barrier. In this study, we used the human neural progenitor cells line ReNcell CX, which was derived from 14-week human cortical brain tissue, as an in vitro model to investigate the neurodevelopmental toxicity effects of BPAF and BPA on ReNcell CX cells, and explored the possible mechanism by which BPAF induced neurodevelopmental toxicity on ReNcell CX cells. The results showed that BPAF reduced the proliferation of neural progenitor cells and changed the differentiation towards neurons after exposure for 24 h. Compared with BPA, ReNcell CX cells are more susceptible to BPAF exposure. In a 3D neurospheres model, BPAF affected the distance that neurons migrated outwards at the concentration of 2 μM. Furthermore, BPAF increased ROS levels in cells and reduced the expression of key proteins in the Nrf2/HO-1 pathway and its downstream molecules, such as SOD, GSH, and CAT. In conclusion, BPAF induces damage to critical nodes in neural progenitor cell development through the Nrf2/HO-1 pathway. Therefore, clarifying its neurodevelopmental toxicity and elaborating on the neurodevelopmental toxicity effects and mechanisms of bisphenol AF will help identify intervention targets for neurodevelopmental toxicity, and will have important public health significance for the safety assessment and risk prediction of bisphenol-related chemicals. Full article

Given its simplicity, Caenorhabditis elegans appears to be a promising model for future research on endocrine disruptors, including bisphenol A and its supposedly safer alternatives. The aim of this study was to investigate the impact of embryonic exposure of C. elegans to different concentrations (0.5, 1.0, and 5 µM) of bisphenol A and its analogs (bisphenol S, bisphenol F, and bisphenol AF) on selected biological characteristics of the nematode C. elegans and to compare them with an unexposed control group. Embryonal exposure of C. elegans to bisphenol A, as well as bisphenol S, F, and AF at concentrations of 0.5, 1.0, and 5 µM resulted in a significant influence on the percentage of hatched eggs and habituation to anterior stimuli (with significant results ranging from p ≤ 0.05 to p ≤ 0.001). The growth of C. elegans was also significantly impaired by bisphenol A, S, and AF in some concentrations (with p-values ranging from p ≤ 0.05 to p ≤ 0.001). Our findings confirm prior research that bisphenol A and its supposedly safer analogs exert a detrimental effect on diverse biological processes. Therefore, bisphenol A analogs should be employed with caution, particularly until a comprehensive risk assessment has been conducted. Full article

In this study, Fe₃O₄ was used as a magnetic core, combined with the characteristics of mesoporous adsorbents, to prepare a novel magnetic mesoporous composite material named MMC. Cetyltrimethylammonium bromide (CTAB) and tetraethyl orthosilicate (TEOS) were used as functional monomers, and a simple etching method was employed. The resulting MMC was used as an effective adsorbent for the magnetic solid-phase extraction of trace residues of six bisphenol endocrine disruptors (bisphenol A, bisphenol B, bisphenol C, bisphenol F, bisphenol AF, and bisphenol AP) from environmental water and food samples. Characterization results indicated that the surface of MMC exhibited a distinct wormhole-like mesoporous structure, with the successful incorporation of CTAB functional groups and Si-OH. The crystal structure of Fe₃O₄ remained stable throughout the preparation process. Mapping analysis confirmed the uniform distribution of CTAB functional groups without aggregation and demonstrated high magnetic intensity, enabling rapid separation and collection under an external magnetic field. Extraction and elution conditions were optimized, and tests were conducted for interfering substances such as humic acid, glucose, fructose, and sucrose under optimal parameters. The results showed that recovery rates were not significantly affected. The quality evaluation of the method demonstrated good linearity, a broad linear range, low limits of detection and quantification, and satisfactory recovery rates. Blank and spiked analyses were conducted for seven real samples, including environmental water (rivers and lakes) and food samples (dairy, juice, and carbonated beverages), with satisfactory spiked recovery rates achieved. Thus, the developed analytical method enables the analysis and detection of trace residues of various bisphenol pollutants in complex matrices, such as environmental water and food samples, providing a valuable reference for trace analysis of similar contaminants in complex matrices. Full article