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锰(manganese,Mn)是一种常见的环境和职业污染物,其主要的毒作用部位是脑。锰神经毒性的主要病变部位位于黑质、纹状体、苍白球和尾状核等,主要表现为锥体外系神经受损。其主要机制之一是由于体内氧化-抗氧化系统的失衡,产生大量的ROS(reactive oxygen species,ROS)引起氧化损伤。谷胱甘肽(glutathione,GSH)是体内重要的抗氧化物质,锰中毒时可以导致GSH合成障碍。核转录因子NF-E2相关因子2(nuclear factor-erythroid 2related factor 2,Nrf2)是一类具有抗氧化特征的转录因子,具有提高内源性GSH水平的作用。本文拟从锰暴露途径和神经毒性、锰与氧化应激、锰中毒对GSH的影响、Nrf2信号通路对锰致GSH合成障碍的调控四个方面作以综述。
Manganese (manganese) is a common environmental and occupational pollutant whose main toxic site is the brain. The main lesions of manganese neurotoxicity located in the substantia nigra, striatum, globus pallidus and caudate nucleus, etc., mainly manifested extrapyramidal nerve damage. One of the main mechanisms is that due to the imbalance of the oxidation-antioxidant system in the body, a large amount of reactive oxygen species (ROS) is caused to cause oxidative damage. Glutathione (GSH) is an important anti-oxidant in the body. Manganese poisoning can lead to the disorder of GSH synthesis. Nuclear factor-erythroid 2 related factor 2 (Nrf2) is a class of transcription factors that have antioxidant properties and has the effect of increasing endogenous GSH levels. In this paper, the effects of manganese exposure and neurotoxicity, manganese and oxidative stress, the effect of manganese poisoning on GSH, and the regulation of Nrf2 signaling pathway on the regulation of manganese-induced GSH synthesis were reviewed.