Bisphenol A (BPA) has been documented as a mediator for a number of health effects, including inflammation, oxidative stress, carcinogenicity, and mood dysfunction. The literature on the role of BPA in inducing altered neurobehavioral response and brain morphology and plausible neuroprotective role of taurine against BPA induced oxidative stress mediated neurotoxicity is limited. Therefore, the present experimental paradigm was set for 21 days to expound the neuroprotective efficacy of taurine against BPA-induced neurotoxicity in zebrafish (Danio rerio) following waterborne exposure. Neurobehavioral studies were conducted by light–dark preference test (LDPT) and novel tank diving test (NTDT). To validate that the neuroprotective efficacy of taurine against BPA-induced neurotoxicity is associated with the modulation of the antioxidant defense system, we have conducted biochemical studies in zebrafish brain. Changes in brain morphology leading to neurobehavioral variations following co-supplementation of BPA and taurine were evaluated by Hoechst staining and cresyl violet staining (CVS) in periventricular gray zone (PGZ) of zebrafish brain. Our findings show that taurine co-supplementation significantly improved the BPA-induced altered scototaxis and explorative behavior of zebrafish. Further, BPA-induced augmented oxidative stress was considerably ameliorated by taurine co-supplementation. Subsequently, our observation also points toward the neuroprotective role of taurine against BPA-induced neuronal pyknosis and chromatin condensation in PGZ of zebrafish brain. In a nutshell, the findings of the current study show the neuroprotective efficacy of taurine against BPA-induced oxidative stress-mediated neurotoxicity. Elucidation of the underlying signaling mechanism of taurine-mediated neuroprotection would provide novel strategies for the prevention/treatment of BPA-persuaded serious neurological consequences.

中文翻译：

---

牛磺酸抑制双酚 A 诱导的氧化应激可促进神经保护并恢复斑马鱼的神经行为反应（Danio rerio）

双酚 A (BPA) 已被证明是多种健康影响的介质，包括炎症、氧化应激、致癌性和情绪障碍。关于 BPA 在诱导神经行为反应和大脑形态改变中的作用以及牛磺酸对 BPA 诱导的氧化应激介导的神经毒性的似是而非的神经保护作用的文献是有限的。因此，本实验范式设定为 21 天，以阐述牛磺酸对 BPA 诱导的斑马鱼神经毒性的神经保护作用 ( Danio rerio) 在水性暴露之后。通过明暗偏好测试（LDPT）和新型坦克潜水测试（NTDT）进行神经行为研究。为了验证牛磺酸对 BPA 诱导的神经毒性的神经保护功效与抗氧化防御系统的调节有关，我们在斑马鱼脑中进行了生化研究。在斑马鱼脑的脑室周围灰区 (PGZ) 中，通过 Hoechst 染色和甲酚紫染色 (CVS) 评估了在共同补充 BPA 和牛磺酸后导致神经行为变化的大脑形态变化。我们的研究结果表明，牛磺酸共同补充显着改善了 BPA 诱导的斑马鱼的 scototaxis 和探索行为的改变。此外，牛磺酸共同补充显着改善了 BPA 诱导的氧化应激增强。随后，我们的观察还指出牛磺酸对斑马鱼脑 PGZ 中 BPA 诱导的神经元固缩和染色质凝聚的神经保护作用。简而言之，当前研究的结果表明牛磺酸对 BPA 诱导的氧化应激介导的神经毒性具有神经保护功效。阐明牛磺酸介导的神经保护的潜在信号机制将为预防/治疗 BPA 引起的严重神经系统后果提供新的策略。