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Bisphenol F is a substitute material for bisphenol A and is widely used in household products as a raw material for polycarbonate resin, epoxy resin, and plastic reinforcement. It is known to be mainly used in food containers, thermal paper for receipts, and coatings for water pipes. In some countries, bisphenol F has been detected in drinking water and human urine samples. However, due to the lack of safety evaluation data on bisphenol F, it is difficult to establish appropriate guidelines for the proper use of the substance, and social anxiety is increasing accordingly. This study investigated the use, exposure route, and distribution flow of bisphenol F, a household chemical. To determine the no-observed-adverse-effect level (NOAEL) and target organ of bisphenol F after exposure, a single-dose oral toxicity, dose-range finding (28 day oral), repeated dose toxicity (90 day oral), and genotoxicity (reverse mutation, chromosomal abnormality, in vivo micronucleus test) tests were performed. The pharmacokinetic profile was also obtained. The test results are as follows: in the pharmacokinetic study, it was confirmed that single oral exposure to BPF resulted in systemic exposure; in single oral dose toxicity test, the approximate lethal dose was found to be 4000 mg/kg and confusion and convulsion was shown in the test animals; NOAEL was determined to be 2 mg/kg/day for male and 5 mg/kg/day for female, and the no-observed-effect level (NOEL) was determined to be 2 mg/kg/day for males and 1 mg/kg/day for females, and the target organ was the small intestine; genotoxicity tests confirmed that BPF does not induce genotoxicity. [ABSTRACT FROM AUTHOR]

Bisphenol A (BPA) is an environmental toxin widely used in manufacturing industries. Studies conducted on the neurotoxicity of BPA demonstrated that at excessive, high concentrations (≥ 200 µM) adverse responses occurred which were not detectable using traditional toxicity tests at lower chemical quantities than 200 µM. Thus, a method capable of effectively detecting neurotoxicity at low concentrations (≤ 100 µM) was devised. Bisphenol A-mediated neurotoxicity was examined in primary cultured neurons using various methods, including Western blot, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) cytotoxicity and reactive oxygen species assays. These methods confirmed BPA-induced toxicity at 200 μM, but no marked effect was observed at concentrations below 200 μM. However, when immunocytochemistry (ICC) was performed using a co-immunofluorescence assay of doublecortin (DCX) and microtubule-associated protein 2 (MAP2), BPA adversely affected neuronal maturation in neural progenitor cells at concentrations as low as 100 µM, at which the three traditional methods failed to detect any neurotoxic effect. Our DCX/MAP2 ICC findings indicate that low concentrations of BPA are toxic to developing neurons, and suggest that the devised double ICC technique might provide an effective means of assessing neurotoxic effects of environmental toxins at low concentrations. [ABSTRACT FROM AUTHOR]

[Display omitted] • BPA, BPS and BPAF were effectively degraded under UV-LED/chlorine reaction. • RCS contributed the most to the removal of BPs, followed by chlorination at pH 6–8. • Radical contribution was dependent on the functional groups and pK a values of BPs. • Chlorinated BPs were major byproducts and these were removed with further reaction. • Ecotoxicity during the removal of BPs under UV-LED/chlorine reaction decreased. We investigated the UV-LED/chlorine reaction for the degradation of bisphenol A (BPA) and its alternatives, bisphenol S (BPS) and bisphenol AF (BPAF) in water. Three bisphenols (BPs) were removed by the pseudo-first-order kinetics. BPA showed the highest removal compared to BPS and BPAF at pH 7 due to the electron-donating isopropyl group in BPA compared to electron-withdrawing sulfonyl and hexafluoro-isopropyl groups in BPS and BPAF, respectively. While the degradation of BPs during the UV-LED/chlorine reaction was contributed mainly by reactive chlorine species (RCS) at pH 6 to 8, and mainly by chlorination reaction at pH 9 due to the different functional groups and pK a values of BPs, and the status of chlorine depending on pHs. While humic acid suppressed the degradation of BPs, HCO 3 − ions generally increased the removal of BPs. Chlorinated BPs (Cl x BPs) were identified as major transformation products (TPs) in the UV-LED/chlorine reaction using LC-QTOF/MS analysis, and these Cl x BPs were effectively removed by further reaction. In addition, >15 minor TPs and three mineralization products (acetate, formate, and chloroform) were identified for each BP degradation. Defluorination (37% in 4 hr) was observed an as the mineralization pathway for BPAF, indicating that UV-LED/chlorine reaction can break the strong C-F bond on BPAF. We proposed the degradation pathways of three BPs based on the identified TPs and theoretical reactive sites calculated using the condensed Fukui function. The major pathways were sequential chlorine substitution, coupling reaction, and hydroxylation reaction. The ECOSAR assessment showed that the UV-LED/chlorine process is effective in lowering the ecotoxicities of BPs and their TPs. [ABSTRACT FROM AUTHOR]

Tetrabromobisphenol A (TBBPA) is a brominated flame retardant that is commonly used in commercial and household products, such as, computers, televisions, mobile phones, and electronic boards. TBBPA can accumulate in human body fluids, and it has been reported that TBBPA possesses endocrine disruptive activity. However, the neurotoxic effect of TBBPA on hippocampal neurogenesis has not yet been investigated. Accordingly, the present study was undertaken to evaluate the effect of TBBPA on adult hippocampal neurogenesis and cognitive function. Male C57BL/6 mice were orally administrated vehicle or TBBPA (20 mg/kg, 100 mg/kg, or 500 mg/kg daily) for two weeks. TBBPA was observed to significantly and dose-dependently reduce the survival of newly generated cells in the hippocampus but not to affect the proliferation of newly generated cells. Numbers of hippocampal BrdU and NeuN positive cells were dose-dependently reduced by TBBPA, indicating impaired neurogenesis in the hippocampus. Interestingly, glial activation without neuronal death was observed in hippocampi exposed to TBBPA. Furthermore, memory retention was found to be adversely affected by TBBPA exposure by a mechanism involving suppression of the BDNF-CREB signaling pathway. The study suggests high dose TBBPA disrupts hippocampal neurogenesis and induces associated memory deficits. [ABSTRACT FROM AUTHOR]

Abstract: Bisphenol A (BPA) is used as a monomer during the manufacture of polycarbonate plastics and epoxy resins. However, BPA adversely affects reproductive organ growth and development, and it has been proposed that the detrimental effects of BPA could extend to future generations. The present study was conducted to evaluate the transgenerational effects of BPA on hippocampal neurogenesis and neurocognitive function. Pregnant female C57BL/6 mice (F0) were exposed to BPA (0.1–10mg/kg) from gestation day 6 to 17, and female offspring (F2) from F1 generation mice were prepared. It was found that exposure of F0 mice to BPA at 10mg/kg decreased the number of newly generated cells in the hippocampi of F2 female mice. Passive avoidance testing revealed that high-doses BPA (1mg/kg and 10mg/kg) decreased cross-over latency time in F2 mice, suggesting a BPA-mediated neurocognitive deficit in terms of memory retention. Furthermore, it was found that levels of phospho-ERK, brain-derived neurotrophic factor (BDNF), and phospho-CREB in hippocampi were significantly lower in F2 mice. Interestingly, the effects of BPA on hippocampal neurogenesis were found to be correlated with altered DNA methylation. In particular, high-dose BPA exposure increased DNA methylation of the CREB regulated transcription coactivator 1 (Crtc1) generated in F2 mice. These findings suggest that BPA exposure of pregnant mothers could adversely affect hippocampal neurogenesis and cognitive function in future generations by modulating the ERK and BDNF–CREB signaling cascades. [Copyright &y& Elsevier]

Abstract: Bisphenol A (BPA) is widely used in the manufacture of plastics and epoxy resins, and is known to affect reproductive organ growth and development. However, the effects of BPA on hippocampal neurogenesis are unclear in young adult mice. Therefore, the present study was conducted to examine the effects of BPA on hippocampal neurogenesis and learning as well as memory performance in young adult mice. BPA (1, 5, and 20mg/kg/day) was administered orally to mice for 2weeks. It was found that high-dose BPA (20mg/kg/day) decreased the number of newly generated cells in hippocampus, but that low-dose BPA (1mg/kg) increased the survival of newly generated cells in hippocampi of young mice. Furthermore, high-dose BPA (20mg/kg/day) was found to impair learning and memory performance significantly. However, no significant differences were observed between high- and low-dose treated mice in terms of levels of brain-derived neurotrophic factor (BDNF) or reactive oxygen species production in hippocampus. In addition, BPA treatment did not induce neuronal loss or damage or astrocyte activation. These data suggest that exposure to BPA causes fluctuations in hippocampal neurogenesis in young adult mice that result in spatial learning and memory impairment via a BDNF-independent pathway. [Copyright &y& Elsevier]