Department of Environmental Health, School of Public Health, China Medical University, No. 77 Puhe Road, Shenyang North New Area, Shenyang 110122, Liaoning, China.
Department of Environmental Health, School of Public Health, China Medical University, No. 77 Puhe Road, Shenyang North New Area, Shenyang 110122, Liaoning, China.
Neuroscience. 2021 Aug 10;469:175-190. doi: 10.1016/j.neuroscience.2021.06.026. Epub 2021 Jun 24.
Methylmercury (MeHg) is a potential neurotoxin that is highly toxic to the human central nervous system. Although MeHg neurotoxicity has been widely studied, the mechanism of MeHg neurotoxicity has not yet been fully elucidated. Some research evidence suggests that oxidative stress and autophagy are important molecular mechanisms of MeHg-induced neurotoxicity. Researchers have widely accepted that oxidative stress regulates the autophagy pathway. The current study reviews the activation of Nuclear factor-erythroid-2-related factor (Nrf2)-related oxidative stress pathways and autophagy signaling pathways in the case of MeHg neurotoxicity. In addition, autophagy mainly plays a role in the neurotoxicity of MeHg through mTOR-dependent and mTOR-independent autophagy signaling pathways. Finally, the regulation of autophagy by reactive oxygen species (ROS) and Nrf2 in MeHg neurotoxicity was explored in this review, providing a new concept for the study of the neurotoxicity mechanism of MeHg.
甲基汞（MeHg）是一种潜在的神经毒素，对人类中枢神经系统具有高度毒性。尽管已经广泛研究了 MeHg 的神经毒性作用，但 MeHg 神经毒性的作用机制尚未完全阐明。一些研究证据表明，氧化应激和自噬是 MeHg 诱导的神经毒性的重要分子机制。研究人员普遍认为，氧化应激调节自噬途径。本研究综述了在 MeHg 神经毒性情况下核因子-红细胞 2 相关因子（Nrf2）相关氧化应激途径和自噬信号通路的激活。此外，自噬主要通过 mTOR 依赖性和 mTOR 非依赖性自噬信号通路在 MeHg 的神经毒性中发挥作用。最后，本文探讨了活性氧（ROS）和 Nrf2 对 MeHg 神经毒性中自噬的调节，为研究 MeHg 的神经毒性机制提供了新的概念。
