Manganese exposure and induced oxidative stress in the rat brain
Manganese exposure and induced oxidative stress in the rat brain
复制标题
DOI：
10.1016/j.scitotenv.2004.04.044
复制
发表时间：
2004-12-01
影响因子：
9.8
通讯作者：
Aschner, M
中科院分区：
文献类型：
--
作者：
Erikson, KM;Dobson, AW;Aschner, M
由于高水平Mn暴露和/或代谢异常（肝病和胆汁排泄减少），可能会发生与脑锰水平过高相关的神经毒性。据报道，脑锰水平升高可诱导氧化应激，以及神经递质代谢的改变，同时伴有神经行为和运动缺陷。锰可以在脑中产生氧化应激的两种假定机制是：（1）通过其对多巴胺的氧化，以及（2）干扰正常的线粒体呼吸。抗氧化剂种类的测量（例如，谷胱甘肽和金属硫蛋白），和大量对氧化非常敏感的蛋白质（酶）（例如，谷氨酰胺合成酶）通常被用作氧化应激的生物标志物，特别是在大鼠脑组织中。本文探讨了锰在大鼠脑神经毒性和氧化应激的共同途径之间的联系。(C)2004年由Elsevier B. V.出版
Neurotoxicity linked to excessive brain manganese levels can occur as a result of high level Mn exposures and/or metabolic aberrations (liver disease and decreased biliary excretion). Increased brain manganese levels have been reported to induce oxidative stress, as well as alterations in neurotransmitter metabolism with concurrent neurobehavioral and motor deficits. Two putative mechanisms in which manganese can produce oxidative stress in the brain are: (1) via its oxidation of dopamine, and (2) interference with normal mitochondrial respiration. Measurements of antioxidant species (e.g., glutathione and metallothionein), and the abundance of proteins (enzymes) exquisitely sensitive to oxidation (e.g., glutamine synthetase) have been commonly used as biomarkers of oxidative stress, particularly in rat brain tissue. This paper examines the link between manganese neurotoxicity in the rat brain and common pathways to oxidative stress. (C) 2004 Published by Elsevier B.V.