Coenzyme Q induces nigral mitochondrial uncoupling and prevents dopamine cell loss in a primate model of Parkinson's disease
Coenzyme Q induces nigral mitochondrial uncoupling and prevents dopamine cell loss in a primate model of Parkinson's disease
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DOI：
10.1210/en.2003-0163
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发表时间：
2003-07-01
期刊：
影响因子：
4.8
通讯作者：
Redmond, DE
中科院分区：
文献类型：
--
作者：
Horvath, TL;Diano, S;Redmond, DE
帕金森病的特征是黑质多巴胺细胞丧失。帕金森病和神经毒素 1-甲基-4-苯基-1,2,5,6 四氢吡啶可能通过氧化应激破坏多巴胺神经元。辅酶 Q 是线粒体解偶联蛋白的辅助因子，可增强 4 态呼吸并消除超氧化物。在此，我们报告在猴子中短期口服辅酶Q可诱导黑质线粒体解偶联，并防止给予猴子1-甲基-4-苯基-1,2,5,6四氢吡啶后多巴胺细胞损失。
Parkinson's disease is characterized by dopamine cell loss of the substantia nigra. Parkinson's disease and the neurotoxin 1-methyl-4-phenyl-1,2,5,6 tetrahydropyridine may destroy dopamine neurons through oxidative stress. Coenzyme Q is a cofactor of mitochondrial uncoupling proteins that enhances state-4 respiration and eliminate superoxides. Here we report that short-term oral administration of coenzyme Q induces nigral mitochondrial uncoupling and prevents dopamine cell loss after 1-methyl-4-phenyl-1,2,5,6 tetrahydropyridine administration in monkeys.