Free radicals and mitochondrial dysfunction in Parkinson's disease.
Free radicals and mitochondrial dysfunction in Parkinson's disease.
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帕金森病中的自由基和线粒体功能障碍。
DOI：
10.1042/bst0210367
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发表时间：
1993
影响因子：
3.9
通讯作者：
J. Cooper
中科院分区：
文献类型：
--
作者：
A. Schapira;A. Hartley;M. Cleeter;J. Cooper
PD中复合物I缺乏与多巴胺能细胞死亡的确切关系及其病因尚不清楚。然而，越来越多的证据表明，这种线粒体缺陷可能在一系列事件中发挥核心作用，最终导致神经神经元的丧失。需要进一步的工作来确定复合物I缺乏的分子机制，因为这些可能为帕金森病的最终原因提供重要的指标。这可能涉及复合体I的遗传异常，可能传递对PD的易感性。另外，外源性或内源性毒性物质可能沿着与MPTP相似的途径靶向黑质复合体I。遗传易感性和环境诱发因素的结合已经获得了大量支持，可以解释帕金森病的原因。
The precise relationship of the complex I deficiency in PD to the dopaminergic cell death and aetiology of this disorder is as yet unknown. However, evidence is accruing that this mitochondrial defect may play a central role in the cascade of events that terminates in nigral neuronal loss. Further work needs to be carried out to determine the molecular mechanisms that underlie the complex I deficiency as these may provide important indicators to the ultimate cause of PD. This may involve a genetic abnormality of complex I that may convey a susceptibility to developing PD. Alternatively, exogenous or endogenous toxic agents may target nigral complex I along pathways similar to those recognized for MPTP. A combination of a genetic predisposition in addition to an environmental precipitant has gained substantial support as an explanation for the cause of PD.