Toxicity Of Bisphenol A Research Articles

Activation of peroxymonosulfate by CuFe2O4-CoFe2O4 composite catalyst for efficient bisphenol a degradation: Synthesis, catalytic mechanism and products toxicity assessment

In this research, the CuFe2O4-CoFe2O4 metallic oxides catalyst (donated as CCF) was synthesized by solvothermal method and applied to degrade bisphenol A (BPA) by activating peroxymonosulfate (PMS). The different influences containing initial PMS concentration, pH, catalyst dosage, coexisting ions and reaction temperature on the degradation efficiency of BPA were systematically investigated. The CCF exhibited 99.3% removal efficiency and 72.5% mineralization of BPA. Notably, compared with the reported metallic catalysts, CCF exhibited much lower amount of metal leaching during the degradation process. The superior catalytic activity and stability of CCF was attributed to the synergistic effects of Co2+/Co3+, Cu+/Cu2+ and Fe2+/Fe3+ redox cycles. The SO4•− and •OH were detected by chemical scavenging and electron paramagnetic resonance (EPR) tests while SO4•− might play a dominant role for BPA degradation. Furthermore, the catalytic mechanism was proposed and analyzed the toxicity of reaction system. The toxicity of BPA and its oxidation intermediates were predicted by ECOSAR model and activity inhibition experiments to demonstrate that BPA was ultimately mineralized as a non-toxic product. This study suggests that the prepared CCF is an efficient and environmentally friendly catalyst for activating PMS, which has an enormous potential application in practical waste water treatment.

An integrative review on the toxicity of Bisphenol A (BPA) released from resin composites used in dentistry

The main aim of this study was to perform an integrative review on the release of bisphenol A (BPA) from resin-matrix composites and potential toxic effects. A bibliographic search was performed on the PubMed platform using the following keywords: "Bisphenol A" OR "BPA" AND "resin composite" OR "composite resin" AND "toxicity" OR "cytotoxicity" OR "release". Inclusion criteria involved in vitro and in vivo studies on the release and toxicity of BPA. Results highlighted the release of BPA from resin-matrix composites due to insufficient polymerization and/or degradation of the polymeric matrix. BPA is part of the organic matrix of resin-matrix composites and may be hydrolysed in human saliva, although studies report that low doses might not be detected by traditional chemical analysis. Studies exposing zebrafish embryos to different concentrations of Bis-GMA, showed 55% mortality at 10μM Bis-GMA while 30% mortality was recorded at 1μM Bis-GMA. In patients, a BPA concentration of around 2.09 × 10-2 μg/ml was found in the saliva after placement of lingual orthodontic retainers with resin-matrix composites. Also, the BPA molecule can be swallowed and absorbed by the oral/gastrointestinal mucosa, which might result in systemic toxicity. The degradation of resin-matrix composites and release of BPA in oral environment are dependent on the organic matrix content and on the polymerization method. A increased release of BPA can lead to the absorption into oral and gastrointestinal mucosa with high risks of local and systemic toxicity.

Occurrence, Profiles and Ecological Risk of Bisphenol Analogues in a Municipal Sewage Treatment Plant.

Due to the strict control on bisphenol A (BPA) in many countries, bisphenol analogues (BPs) are being widely used as alternative materials to manufacture epoxy resins and polycarbonate plastics, resulting in their occurrence in sewage treatment plants (STPs). In this study, the occurrence and distribution of 7 BPs in a large-scale STP in Beijing China was investigated. Wastewater samples were collected from the influents and effluents of each processing unit, and extracted by solid-phase extraction. Target compounds were quantified by ultra-performance liquid chromatography tandem mass spectrometry (HPLC-MS/MS). The total concentrations of seven BPs (ΣBPs) were 400.42 ± 48.12ng/L in the raw sewage, 438.60 ± 46.50ng/L in the primary effluent, 17.21 ± 13.12ng/L in the secondary effluent, and 11.33 ± 4.84ng/L in the tertiary effluent, respectively. Bisphenol S (BPS) and BPA were the predominant congener in raw sewage with an overall contribution of 29.32% and 70.22% to the ΣBPs, indicating that there was a large amount of BPS and BPA consumption in the study area. During a one-week sampling period, ΣBPs changed slightly at the same sampling site. It was found that high removal efficiencies were achieved for BPs in anoxic and oxic secondary clarifier treatment units, suggesting that biodegradation and sorption played major roles in BPs elimination in the STP. After tertiary treatment, all BPs except BPA were completely removed, suggesting the necessity to investigate the fate and toxicity of BPA in the aquatic environment.

Bisphenol A, Bisphenol F, and Bisphenol S: The Bad and the Ugly. Where Is the Good?

Background: Bisphenol A (BPA), a reprotoxic and endocrine-disrupting chemical, has been substituted by alternative bisphenols such as bisphenol F (BPF) and bisphenol S (BPS) in the plastic industry. Despite their detection in placenta and amniotic fluids, the effects of bisphenols on human placental cells have not been characterized. Our objective was to explore in vitro and to compare the toxicity of BPA to its substitutes BPF and BPS to highlight their potential risks for placenta and then pregnancy. Methods: Human placenta cells (JEG-Tox cells) were incubated with BPA, BPF, and BPS for 72 h. Cell viability, cell death, and degenerative P2X7 receptor and caspases activation, and chromatin condensation were assessed using microplate cytometry and fluorescence microscopy. Results: Incubation with BPA, BPF, or BPS was associated with P2X7 receptor activation and chromatin condensation. BPA and BPF induced more caspase-1, caspase-9, and caspase-3 activation than BPS. Only BPF enhanced caspase-8 activity. Conclusions: BPA, BPF, and BPS are all toxic to human placental cells, with the P2X7 receptor being a common key element. BPA substitution by BPF and BPS does not appear to be a safe alternative for human health, particularly for pregnant women and their fetuses.

Bisphenol A Exposure Disrupts Organelle Distribution and Functions During Mouse Oocyte Maturation.

Bisphenol A (BPA) is one of the ubiquitous environmental endocrine disruptors (EEDs). Previous studies have shown that the reproduction toxicity of BPA could cause severe effects on the mammal oocytes and disturb the quality of mature oocytes. However, the toxic effects of BPA on the organelles of mouse oocytes have not been reported. In this study, to investigate whether BPA can be toxic to the organelles, we used different concentrations of BPA (50, 100, and 200 μM) to culture mouse oocytes in vitro. The results showed that 100 μM BPA exposure could significantly decrease the developmental capacity of oocytes. Then, we used the immunofluorescence staining, confocal microscopy, and western blotting to investigate the toxic effects of BPA on the organelles. The results revealed that mitochondrial dysfunction is manifested by abnormal distribution and decreased mitochondrial membrane potential. Moreover, the endoplasmic reticulum (ER) is abnormally distributed which is accompanied by ER stress showing increased expression of GRP78. For the Golgi apparatus, BPA-exposed dose not disorder the Golgi apparatus distribution but caused abnormal structure of Golgi apparatus, which is manifested by the decrease of GM130 protein expression. Moreover, we also found that BPA-exposed led to the damage of lysosome, which were shown by the increase of LAMP2 protein expression. Collectively, our findings demonstrated that the exposure of BPA could damage the normal function of the organelles, which may explain the reduced maturation quality of oocytes.

Bisphenol A exposure induces apoptosis and impairs early embryonic development in Xenopus laevis.

Bisphenol A (BPA), an endocrine-disrupting chemical that is largely produced and used in the plastics industry, causes environmental pollution and is absorbed by humans through consumption of food and liquids in polycarbonate containers. BPA exerts developmental and genetic toxicities to embryos and offsprings, but the embryotoxicity mechanism of this chemical is unclear. This study aimed to explore the toxic effect of BPA on embryonic development and elucidate its toxicity mechanism. Embryos of Xenopus laevis as a model were treated with different concentrations (0.1, 1, 10, and 20μM) of BPA at the two-cell stage to investigate the developmental toxicity of BPA. Embryonic development and behaviors were monitored 24h-96h of BPA exposure. BPA concentrations greater than 1μM exerted significant teratogenic effects on the Xenopus embryos, which showed short tail axis, miscoiled guts, and bent notochord as the main malformations. The 20μM BPA-treated embryos were seriously damaged in all aspects and exhibited deformity, impaired behavioral ability, and tissue damage. The DNA integrity and apoptosis of the Xenopus embryos were also investigated. Exposure to BPA concentrations higher than 0.1μM significantly induced DNA damage (p<0.05). The 10 and 20μM BPA-treated embryos exhibited higher levels of cleaved caspase-3 protein than the control. The ratios of bax/bcl-2 mRNA were significantly higher in the 10μM and 20μM-treated embryos than the ratio in the control group. Overall, data indicated that BPA can delay the early development, induce DNA damage and apoptosis, and eventually cause multiple malformations in Xenopus embryos.

The orphan nuclear receptor Nur77 plays a vital role in BPA-induced PC12 cell apoptosis

Bisphenol A (BPA) is a typical environmental endocrine disruptor that can migrate into organisms through skin contact, breathing, diet and various other approaches. The reproductive toxicity and neurotoxicity of BPA has been confirmed by several toxicological studies. However, the neurotoxicity of BPA is still controversial. In the present study, we used PC12 cells as a model to investigate the mechanism of BPA-induced neuronal apoptosis. BPA exposure reduced cell viability, altered cell morphology and aggravated intracellular Lactate dehydrogenase (LDH) release, intracellular Ca2+ concentration, Reactive oxygen species (ROS) levels, apoptosis and the reduction in the mitochondrial transmembrane potential (ΔΨm). Moreover, the results of the Western blot (WB) and Real-time quantitative polymerase chain reaction (RT-qPCR) assays indicated that the expression levels of Nur77 in the BPA group were down-regulated and accompanied by the downregulation of the NF-κb/Bcl-2 proteins and the upregulation of cleaved-caspase 3, which is a marker of apoptosis. However, these changes were significantly reversed with the upregulation of the Nur77 protein by introducing plasmids carrying the nur77 gene. These results indicated that BPA-induced apoptosis was closely related to Nur77-mediated inhibition of the NF-κb/Bcl-2 pathway.

Bisphenol A removal and degradation pathways in microorganisms with probiotic properties

Bisphenol-A (BPA) is a constituent of polycarbonate plastics and epoxy resins, widely applied on food packaging materials. As BPA exposure results in health hazards, its efficient removal is of crucial importance. In our study five potentially probiotic microorganisms, namely Lactococcus lactis, Bacillus subtilis, Lactobacillus plantarum, Enterococcus faecalis, and Saccharomyces cerevisiae, were tested for their toxicity tolerance to BPA and their BPA removal ability. Although BPA toxicity, evident on all microorganisms, presented a correlation to both BPA addition time and its concentration, all strains exhibited BPA-removal ability with increased removal rate between 0 and 24 h of incubation. BPA degradation resulted in the formation of two dimer products in cells while the compounds Hydroquinone (HQ), 4-Hydroxyacetophenone (HAP), 4-Hydroxybenzoic acid (HBA) and 4-Isopropenylphenol (PP) were identified in the culture medium. In the proposed BPA degradation pathways BPA adducts formation appears as a common pattern, while BPA decomposition as well as the formation, and the levels of its end products present differences among microorganisms. The BPA degradation ability of the tested beneficial microorganisms demonstrates their potential application in the bioremediation of BPA contaminated foods and feeds and provides a means to suppress the adverse effects of BPA on human and animal health.

Neuroendocrine disruption by bisphenol A and/or di(2-ethylhexyl) phthalate after prenatal, early postnatal and lactational exposure.

Bisphenol A (BPA) and di(2-ethylhexyl)phthalate (DEHP) are abundant endocrine disrupting chemicals (EDCs). In recent years, studies showed that EDCs may lead to neurodevelopmental diseases. The effects of prenatal exposure to these chemicals may have serious consequences. Moreover, exposure to EDCs as a mixture may have different effects than individual exposures. The present study aimed to determine the toxicity of BPA and/or DEHP on central nervous system (CNS) and neuroendocrine system in prenatal and lactational period in Sprague-Dawley rats. Pregnant rats were randomly divided into four groups: control (received vehicle); BPA group (received BPA at 50mg/kg/day); DEHP group (received DEHP at 30mg/kg/day); and combined exposure group (received both BPA at 50mg/kg/day and DEHP at 30mg/kg/day) during pregnancy and lactation by oral gavage. At the end of lactation, male offspring (n = 6) were randomly grouped. The alterations in the brain histopathology, neurotransmitter levels and enzyme activities in the cerebrum region, oxidative stress markers, and apoptotic effects in the hippocampus region were determined at adulthood. The results showed that exposure to EDCs at early stages of life caused significant changes in lipid peroxidation, total GSH and neurotransmitter levels, and activities of neurotransmitter-related enzymes. Moreover, BPA and/or DEHP led to apoptosis and histopathologic alterations in the hippocampus. Therefore, we can suggest that changes in oxidant/antioxidant status, as well as in neurotransmitters and related enzymes, can be considered as the underlying neurotoxicity mechanisms of BPA and DEHP. However, more mechanistic studies are needed.

Evaluation of testicular toxicity upon fetal exposure to bisphenol A using an organ culture method

Humans are exposed to a multitude of endocrine disruptor chemicals (EDCs) that can interfere with the action of endogenous hormones and the normal development of reproductive organs. Bisphenol A (BPA) is one of the most common EDCs found in the environment. Here, we evaluated BPA toxicity on fetal testes using an in vitro organ culture system. Mouse fetal testes sampled at 15.5 days post coitus were cultured in a medium containing BPA for 5 days. The number of germ cells was reduced by BPA treatment, whereas the number of Sertoli cells was slightly increased by BPA at the highest dose (100 μM). Consistently, BPA treatment reduced the protein and gene expression levels of germ cell markers, but it increased the expression levels of Sertoli cell markers. The expression levels of fetal Leydig cell markers such as Cyp11a1, Thbs2, Cyp17a1, and Pdgf-α were significantly increased, whereas those of adult Leydig cell markers such as Hsd17b3, Ptgds, Sult1e1, Vcam1, and Hsd11b1 were decreased in the testes exposed to BPA. Generally, Notch signaling restricts Leydig cell differentiation from progenitor cells during fetal testis development. The expression levels of Notch1, Notch2, Notch3, Hes1, Ptch1, Jag1, Jag2, c-Myc, Hey1, and Hey2, which are involved in Notch signaling, were markedly higher in BPA-treated fetal testes than in the controls, indicating that BPA interrupts fetal Leydig cell development. BPA also disrupted steroidogenesis in the fetal testis organ culture system. In conclusion, our study showed that BPA inhibits fetal germ cell growth, Leydig cell development, and steroidogenesis.

Mechanisms for the impacts of graphene oxide on the developmental toxicity and endocrine disruption induced by bisphenol A on zebrafish larvae

The huge production and application of bisphenol A (BPA) and graphene oxide (GO) inevitably lead to their co-presence in aquatic ecosystems, which might cause joint toxic effects to aquatic organisms. Herein, zebrafish larvae at 3 d post fertilization (dpf) were exposed to BPA, GO, and their mixtures until 7 dpf. GO was ingested and localized in the gut. 5000 μg/L BPA alone induced distinct ultrastructure damage, which was alleviated by GO, indicating that GO reduced the developmental toxicity of BPA. The levels of endocrine-related genes and steroid hormones were all modulated to the greatest extent by 500 μg/L BPA, suggesting that BPA exhibited a remarkable endocrine disruption effect. However, the responses of some of these genes were recovered by GO, indicating that GO also alleviated the BPA-induced endocrine disruption. The mRNA levels of five genes in the extracellular matrix-receptor interaction pathway, two in the oxidative phosphorylation pathway, 18 in the metabolic pathways, and five in the peroxisome proliferator-activated receptor signaling pathway were distinctly altered by 5000 μg/L BPA, but most of them were recovered in the presence of GO. GO might relieve the BPA-induced developmental toxicity and endocrine disruption by recovering the genes related to the corresponding pathways.

Release and toxicity of bisphenol-A (BPA) contained in orthodontic adhesives: A systematic review

The objectives of this systematic review of the literature are to search for BPA release from biomaterials used in orthodontics and to highlight their possible impact on human health. Using the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) model, digital and manual searches were conducted in February 2020 in the database of CENTRAL, MEDLINE and EMBASE. Thirteen parameters relating to the release and biological effects of BPA were identified and analysed. Thirty-one non-randomized clinical trials were included. In general, the level of evidence was low, and the risk of bias ranged from moderate to high. Furthermore, although at different concentrations, most of in vitro and in vivo studies found BPA release from orthodontic adhesives. The lack of standardized protocols and the clinical and methodological heterogeneity of the studies prevented a valid interpretation of the actual results. Concerning the possible toxicity of BPA, no conclusive scientific evidence could be drawn, but it seems that orthodontic biomaterials containing BPA have potential adverse biological effects in humans. Until we have solid evidence from clinical trials, clinicians should consider that orthodontic adhesives containing BPA have potential short- and long-term adverse biological effects in humans. Careful consideration should therefore be given to bonding, polymerization and debonding protocols in orthodontics.

Acute toxicity of Bisphenol A (BPA) to tropical marine and estuarine species from different trophic groups.

BPA is chemical pollutant of very high concern due to its toxicity to the environment and risks for human health. Environmental concern consists in BPA entrance into aquatic ecosystems due to acute and chronic toxicity to invertebrates and vertebrates. This study aimed to determine acute BPA toxicity to tropical estuarine-marine species of four trophic levels and integrate BPA toxicity values using species sensitivity distribution (SSD) analysis. Our hypothesis is that BPA toxicity increases towards higher trophic levels. Microalga (Tetraselmis sp.), zooplanktonic grazer (Artemia salina), deposit-feeder invertebrate (Heleobia australis), and omnivorous fish (Poecilia vivipara) were chosen as experimental models. Tetraselmis sp. showed the highest BPA tolerance, without a concentration-dependent response. Species sensitivity have increased from A.salina (LC50,96h=107.2mg L-1), followed by H.australis (LC50,96h=11.53.5mg L-1), to P.vivipara (LC50,96h=3.5mg L-1). Despite the toxicity hierarchy towards trophic levels, which partially supported our hypothesis, SSD did not evidence a clear pattern among estuarine-marine trophic groups. Our study disclosed the sensitivity of not yet investigated species to BPA and, in an integrative way, highlighted BPA toxic effects at different trophic levels. Although estimated acute hazardous concentration (HC5=1.18mgL-1) for estuarine and marine species was higher than environmentally relevant concentrations, sublethal adverse effects induced by BPA exposure may lead to unbalances in population levels and consequently affect the ecological functioning of tropical coastal systems.

Genes regulating development and behavior exhibited altered expression in Drosophila melanogaster exposed to bisphenol A: use of real-time quantitative PCR (qRT-PCR) and droplet digital PCR (ddPCR) in genotoxicity study.

Toxicity of bisphenol A on morphological and life-history traits of model insect Drosophila melanogaster was reported in our previous work. In the present study, we have analyzed the adversity of bisphenol A on the reproductive behavior of adult and on the expression of selected genes in the larva and adult stage of fruit fly exposed to bisphenol A (0.007 g/2 ml. or 3.5 mg/ml), in addition to determination of LC50 value of bisphenol A in larva and pupal stage. We employed both the quantitative reverse transcriptase PCR and droplet digital PCR for analyzing the expression profile of seven genes namely, decapentaplegic, vestigial, wingless, foraging, insulin-like receptor, doublesex, and fruitless.We found bisphenol Ahas more adverse effects on male sexual behavior than females. Moreover, we observed significant downregulation of all the selected genes in treated larvaeexcept, fruitless in male where it showed significant upregulation. On contrary amongthe treated adult flies, significant downregulation of all target genes in both sexes is evident, except, doublesex and fruitless in males which showed significant upregulation. We did not observe any deviation of male: female sexratio from 1:1 under bisphenol A exposure. All these results suggest bisphenol A adversely affects the optimum functioning of genes which are involved in the regulation of metabolic pathways, behavioral pattern, stress response, endocrine homeostasis, neural functioning, and the development of the specific organ in Drosophila melanogaster. Our result not only provides a foundation to study further the bisphenol Atoxicity on different pivotal genes in Drosophila but also suggests the use of the droplet digital PCR technology in toxicity measurement at the molecular level in eukaryotic model systems.

Micropillar/Microwell Chip Assessment for Detoxification of Bisphenol A with Korean Pear (Pyrus pyrifolia).

A micropillar/microwell chip platform with 3D cultured liver cells has been used for HTP screening of hepatotoxicity of bisphenol A (BPA), an endocrine-disrupting chemical. We previously found the hepatotoxicity of BPA is alleviated by alcohol dehydrogenase (ADH) and aldehyde dehydrogenase 2 (ALDH2). In this study, we have tested potential BPA detoxification with Korean pear (Pyrus pyrifolia) extract, stimulators of ADH and ALDH, as well as arbutin, a reference compound in the pears, on the micropillar/microwell chip platform with human liver cells. Surprisingly, the toxicity of BPA was reduced in the presence of Korean pear extract, indicated by significantly increased IC50 values. The IC50 value of BPA with Korean pear extract tested against HepG2 cells was shifted from 151 to 451 μM, whereas those tested against Hep3B cells was shifted from 110 to 204 μM. Among the tested various concentrations, 1.25, 2.5, and 5 mg/mL of the extract significantly reduced BPA toxicity (Ps < 0.05). However, there was no such detoxification effects with arbutin. This result was supported by changes in protein levels of ADH in the liver cells.

Bisphenol A impairs reproductive fitness in zebrafish ovary: Potential involvement of oxidative/nitrosative stress, inflammatory and apoptotic mediators

Bisphenol A (BPA) is a highly pervasive chemical in consumer products with its ascribed endocrine-disrupting properties. Several studies have shown the cytotoxic, genotoxic, and carcinogenic property of BPA over a multitude of tissues. Although BPA exposure has earlier been implicated in female infertility, the underlying molecular mechanisms explaining the toxicity of BPA in the ovary remains less understood. In the present study, a plausible correlation between redox balance or inflammatory signaling and reproductive fitness upon BPA exposure has been examined in zebrafish (Danio rerio) ovary. Congruent with significant alteration of major antioxidant enzymes (SOD1, SOD2, catalase, GPx1α, GSTα1) at the transcript level, 30 d BPA exposure at environmentally relevant concentrations (1, 10 and 100 μg L−1) promotes ovarian ROS/RNS synthesis, lipid peroxidation but attenuates catalase activity indicating elevated stress response. BPA promotes a sharp increase in ovarian p38 MAPK, NF-κB phosphorylation (activation), inducible nitric oxide synthase (Nos2a), and pro-inflammatory cytokines (TNF-α and IL-1β) expression, the reliable markers for inflammatory response. Congruent to an increased number of atretic follicles, BPA-exposed zebrafish ovary reveals elevated Bax/Bcl2 ratio, activation of caspase-8, -3 and DNA breakdown suggesting heightened cell death. Importantly, significant alteration in nuclear estrogen receptor (ER) transcripts (esr1, esr2a, and esr2b) and proteins (ERα, ERβ), gonadotropin receptors, and markers associated with steroidogenesis and growth factor gene expression in BPA-exposed ovary correlates well with impaired ovarian functions and maturational response. Collectively, elevated oxidative/nitrosative stress-mediated inflammatory response and altered ER expression can influence ovarian health and reproductive fitness in organisms exposed to BPA environment.

The effects of bisphenol A, F and their mixture on algal and cyanobacterial growth: from additivity to antagonism.

Bisphenol A (BPA) is, due to its widespread use including the production of plastic materials, an ubiquitous pollutant in the aquatic environment. Due to evidence of adverse BPA effects on the environment and human health, its use has been restricted and replaced by analogues such as bisphenol F (BPF). This study examined the toxicity of BPA, BPF and their mixture towards primary producers, the eukaryotic green alga Pseudokirchneriella subcapitata and the prokaryotic cyanobacterium Synechococcus leopoliensis. The results demonstrated that S. leopoliensis is more sensitive than P. subcapitata, whereas toxic potential of the two BPs is comparable and represents comparable hazard for phytoplankton. The toxicity of the binary mixture was predicted by different models (concentration addition, independent action, combination index and the isobologram method) and compared to experimental data. Additive effect was observed in P. subcapitata over the whole effect concentration range (EC5-EC90), whereas in S. leopoliensis, no pronounced combined effect was observed. The environmental risk characterisation based on the comparison of reported concentrations of BPA and BPF in surface waters to the predicted no-effect concentration values obtained in this study showed that at certain industrial areas, BPA represents environmental risk, whereas BPF does not. However, BPF concentrations in aquatic environment are expected to increase in the future. To enable environmental risk assessment of BP analogues, more data on the toxicity to aquatic species, including combined effect, as well as data on their occurrence in the aquatic environment are needed.Graphical abstract.

Evaluation of green tea extract and epigallocatechin gallate effects on bisphenol A-induced vascular toxicity in isolated rat aorta and cytotoxicity in human umbilical vein endothelial cells.

This study was designed to assess bisphenol A (BPA)-induced vascular toxicity, the effectiveness of green tea extract and epigallocatechin gallate (EGCG) against BPA toxicity, and possible underlying mechanisms. In isolated rat aorta, contractile and relaxant responses as well as malondialdehyde levels were evaluated. Cell viability and effects on the protein levels of apoptotic (bax, bcl2, and caspase-3), autophagic (LC3), and cell adhesion molecules were calculated using the MTT method and western blotting in human umbilical vein endothelial cells (HUVECs). BPA increased aorta MDA levels (p < .0001) and decreased vascular responses to KCl [20 and 40 mM (p < .0001), 80 mM (p < .001)], phenylephrine [10-8 , 10-6 , and 10-5 M (p < .001), 10-7 and 10-4 M (p < .0001)], and acetylcholine [10-6 M (p < .01), 10-5 and 10-4 M (p < .0001)]. In HUVECs, BPA enhanced the levels of LC3A/B, bax/bcl2 ratio, cleaved caspase-3, and vascular cell adhesion molecule-1. Green tea extract, EGCG, and vitamin E co-treatment with BPA diminished the toxic effects of BPA. These findings provide evidence that green tea extract and EGCG possess beneficial effects in preventing BPA-induced vascular toxicity through increasing the antioxidant activities and the regulation of signaling pathways.

Bioaccumulation and reproductive toxicity of bisphenol A in male-pregnant seahorse (Hippocampus erectus) at environmentally relevant concentrations

Seahorses, with brood pouch in adult males, are a bioindicator species that exhibit specialized reproductive strategy of “male pregnancy”. Bisphenol A (BPA), one of the most pervasive endocrine-disrupting chemicals (EDCs), is hazardous for reproductive, immune, and neurological systems. However, no evidence of BPA toxicity to the male-pregnant animals is available. Herein, the reproductive toxicity of BPA was evaluated in lined seahorses (Hippocampus erectus) following exposure to environmentally relevant concentrations (10, 100, and 1000 μg/L) through physiological, histological, and transcriptional analyses. Our results indicated BPA bioaccumulation to be positively correlated with exposure doses in both sexes. Ovarian failure was only observed in the high-dose BPA treatment group, accompanied by the apoptosis of follicular cells and up-regulation of pro-apoptotic genes. However, brood pouches maintenance were surprisingly inhibited at low concentration, and transcriptomic analysis revealed disturbed profiles of genes involved in the extracellular matrix and cell-cell adhesion pathways. Interestingly, seahorse testes were less sensitive to BPA exposure than that in other teleosts. Thus, our study suggests that BPA at environmentally relevant concentrations might cause reproductive dysfunction in seahorses, potentially exerting adverse effects on the seahorse population since most of them inhabit shallow coastal areas with prevalent estrogenic contaminants.

Ultrafast microwave assisted development of magnetic carbon microtube from cotton waste for wastewater treatment

The effect of UVA-Vis irradiation of magnetic microtubes derived from cotton waste on the process of Bisphenol A (BPA) removal and mineralisation is studied. The magnetic microtubes were developed by ultra-fast microwave treatment of carbonised cotton waste to grow Fe3O4 nanoparticles onto the surface of tubes. The activity of magnetic microtubes was tested in the removal of BPA, both in the dark adsorption and under UVA-Vis irradiation. The highest dark adsorption capacity was measured for sample carbonized at 1100 °C (208 mg·g-1), confirming its high potential in BPA removal from water through direct adsorption. The highest changes in water pollution were observed during the first 10 min of treatment. Toxicity of BPA was significantly reduced after treatment and applied procedures enabled the high quality non-toxic water. The obtained results clearly indicate that the ultrafast and solvent free magnetisation of carbon microtube derived from textile waste offers a low-cost solution for the efficient photo mineralisation of BPA.