Guangzhou Key Laboratory of Subtropical Biodiversity and Biomonitoring, School of Life Sciences, South China Normal University, Guangzhou, 510631, China.
Guangzhou Key Laboratory of Subtropical Biodiversity and Biomonitoring, School of Life Sciences, South China Normal University, Guangzhou, 510631, China.
Chemosphere. 2021 Feb;264(Pt 1):128450. doi: 10.1016/j.chemosphere.2020.128450. Epub 2020 Sep 28.
BPA analogs, including bisphenol S (BPS) and bisphenol B (BPB), have been used to replace BPA since it was banned to be added. To investigate whether BPA and its analogs cause oxidative damage effects on primary hippocampal neurons of rats, reactive oxygen species (ROS), malondialdehyde (MDA), superoxide dismutase (SOD), mitochondrial membrane potential (MMP), apoptosis and cell viability assays were conducted after hippocampal neurons exposure to different concentrations of BPA, BPS, and BPB (1, 10, 100 nM and 1, 10, 100 μM). Moreover, the effects of EGCG (5 and 6 μM for male and female, respectively) added on neurons exposed to BPA were assessed. Results showed that 24 h exposure to these bisphenols (BPs) could increase the levels of ROS and contents of MDA, but reduce the activity of SOD significantly. A decline of cell viabilities accompanied with the increasing of apoptosis rates was observed after 7 d exposure to BPs and the reduction of MMP was also observed after 7 d exposure to BPA. Interestingly, BPS has the lower toxicity to hippocampal neurons compared with BPA and BPB. Non-monotonic dose-effect relationships between the concentrations of BPs and the cytotoxic effects were observed, and the effects of BPs on male hippocampal neurons are greater than those of female ones in general. While EGCG can protect neurons free of oxidative damages. In conclusion, the results suggest that BPs may induce sex-specific neurotoxic effects involving oxidative stress, which can be attenuated by EGCG, and males are more sensitive to BPs than females.
双酚 A 类似物，包括双酚 S（BPS）和双酚 B（BPB），自被禁止添加以来，已被用于替代双酚 A。为了研究双酚 A 及其类似物是否对大鼠海马神经元造成氧化损伤，在海马神经元暴露于不同浓度的双酚 A、BPS 和 BPB（1、10、100 nM 和 1、10、100 μM）后，进行了活性氧（ROS）、丙二醛（MDA）、超氧化物歧化酶（SOD）、线粒体膜电位（MMP）、细胞凋亡和细胞活力测定。此外，还评估了 EGCG（雄性和雌性分别为 5 和 6 μM）添加到暴露于双酚 A 的神经元上的效果。结果表明，24 小时暴露于这些双酚（BPs）会增加 ROS 水平和 MDA 含量，但显著降低 SOD 活性。在暴露于 BPs 7 天后，观察到细胞活力下降，凋亡率增加，同时在暴露于 BPA 7 天后，MMP 也降低。有趣的是，与 BPA 和 BPB 相比，BPS 对海马神经元的毒性较低。在 BPs 浓度与细胞毒性作用之间观察到非单调剂量-效应关系，BPs 对雄性海马神经元的作用一般大于对雌性的作用。而 EGCG 可以保护神经元免受氧化损伤。总之，结果表明 BPs 可能引起涉及氧化应激的性别特异性神经毒性作用，EGCG 可以减轻这种作用，而且雄性对 BPs 的敏感性高于雌性。
