Qin Ziyu, Chen Yuqing, Zhao Xinyuan, Yu Shali
Department of Occupational Medicine and Environmental Health, School of Public Health, Nantong University, Nantong Municipal Key Laboratory of Environmental Toxicology, Nantong 226019, Jiangsu Province, China.
Zhejiang Da Xue Xue Bao Yi Xue Ban. 2024 Dec 25;53(6):699-707. doi: 10.3724/zdxbyxb-2024-0127.
It has been confirmed that exposure to various metal pollutants can induce neurotoxicity, which is closely associated with the occurrence and development of neurological disorders. Ferroptosis is a form of cell death in response to metal pollutant exposure and it is closely related to oxidative stress, iron metabolism and lipid peroxidation. Recent studies have revealed that ferroptosis plays a significant role in the neurotoxicity induced by metals such as lead, cadmium, manganese, nickel, and antimony. Lead exposure triggers ferroptosis through oxidative stress, iron metabolism disorder and inflammation. Cadmium can induce ferroptosis through iron metabolism, oxidative stress and ferroptosis related signaling pathways. Manganese can promote ferroptosis through mitochondrial dysfunction, iron metabolism disorder and oxidative stress. Nickel can promote ferroptosis by influencing mitochondrial function, disrupting iron homeostasis and facilitating lipid peroxidation in the central nervous system. Antimony exposure can induce glutathione depletion by activating iron autophagy, resulting in excessive intracellular iron deposition and ultimately causing ferroptosis. This article reviews the effects of metal pollutants on ferroptosis-related indicators and discusses the specific mechanisms by which each metal triggers ferroptosis. It provides a reference for identifying targets for preventing neurotoxicity and for developing treatment strategies for neurological disorders.
已证实,接触各种金属污染物可诱发神经毒性,这与神经疾病的发生和发展密切相关。铁死亡是一种因接触金属污染物而引发的细胞死亡形式,它与氧化应激、铁代谢和脂质过氧化密切相关。最近的研究表明,铁死亡在铅、镉、锰、镍和锑等金属诱发的神经毒性中起重要作用。铅暴露通过氧化应激、铁代谢紊乱和炎症触发铁死亡。镉可通过铁代谢、氧化应激和铁死亡相关信号通路诱导铁死亡。锰可通过线粒体功能障碍、铁代谢紊乱和氧化应激促进铁死亡。镍可通过影响线粒体功能、破坏铁稳态和促进中枢神经系统脂质过氧化来促进铁死亡。锑暴露可通过激活铁自噬诱导谷胱甘肽耗竭,导致细胞内铁过度沉积,最终引起铁死亡。本文综述了金属污染物对铁死亡相关指标的影响,并探讨了每种金属触发铁死亡的具体机制。它为确定预防神经毒性的靶点和制定神经疾病的治疗策略提供了参考。