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2018 Jun 20; 28(18): 1669–1703.
2018年6月20日; 28(18):1669-1703。
Published online 2018 Jun 20. doi: 10.1089/ars.2017.7272 IF: 5.9 Q1 B2
PMCID: PMC5962337 IF: 5.9 Q1 B2

Neurotoxicity Linked to Dysfunctional Metal Ion Homeostasis and Xenobiotic Metal Exposure: Redox Signaling and Oxidative Stress
与金属离子稳态功能失调和异生金属暴露相关的神经毒性:氧化还原信号和氧化应激

Associated Data 相关数据

Supplementary Materials 补充材料

Abstract 抽象的

Significance: Essential metals such as copper, iron, manganese, and zinc play a role as cofactors in the activity of a wide range of processes involved in cellular homeostasis and survival, as well as during organ and tissue development. Throughout our life span, humans are also exposed to xenobiotic metals from natural and anthropogenic sources, including aluminum, arsenic, cadmium, lead, and mercury. It is well recognized that alterations in the homeostasis of essential metals and an increased environmental/occupational exposure to xenobiotic metals are linked to several neurological disorders, including neurodegeneration and neurodevelopmental alterations.
意义:铜、铁、锰和锌等必需金属在涉及细胞稳态和生存以及器官和组织发育的多种过程的活动中发挥着辅助因子的作用。在我们的一生中,人类还接触来自天然和人为来源的外来金属,包括铝、砷、镉、铅和汞。众所周知,必需金属稳态的改变和外源金属环境/职业暴露的增加与多种神经系统疾病有关,包括神经变性和神经发育改变。

Recent Advances: The redox activity of essential metals is key for neuronal homeostasis and brain function. Alterations in redox homeostasis and signaling are central to the pathological consequences of dysfunctional metal ion homeostasis and increased exposure to xenobiotic metals. Both redox-active and redox-inactive metals trigger oxidative stress and damage in the central nervous system, and the exact mechanisms involved are starting to become delineated.
最新进展:必需金属的氧化还原活性是神经元稳态和大脑功能的关键。氧化还原稳态和信号传导的改变是金属离子稳态功能失调和外源金属暴露增加的病理后果的核心。氧化还原活性和氧化还原非活性金属都会引发中枢神经系统的氧化应激和损伤,并且所涉及的确切机制已开始被阐明。

Critical Issues: In this review, we aim to appraise the role of essential metals in determining the redox balance in the brain and the mechanisms by which alterations in the homeostasis of essential metals and exposure to xenobiotic metals disturb the cellular redox balance and signaling. We fo