Cooper J M, Daniel S E, Marsden C D, Schapira A H
Department of Clinical Neurosciences, Royal Free Hospital School of Medicine, London, England, U.K.
Mov Disord. 1995 May;10(3):295-7. doi: 10.1002/mds.870100311.
There is evidence for a 37% deficiency of complex I activity in Parkinson's disease (PD), which appears to be specific for PD amongst parkinsonian syndromes and selective for the substantia nigra within the central nervous system. Rat studies have shown that, in the context of a normal nigrostriatal dopaminergic cell population, L-dihydroxyphenylalanine (L-dopa) causes a reversible 25% defect of complex I activity in nigral and striatal tissue. Analysis of striatal tissue from PD patients after prolonged exposure to high-dose L-dopa does not show such a defect. Results of these and other studies suggest that L-dopa therapy does not cause complex I deficiency in PD striatum. However, it cannot be excluded that, in the particular environment of the PD substantia nigra, L-dopa may enhance a preexisting complex I defect.
有证据表明，帕金森病（PD）患者中复合物I活性存在37%的缺陷，这在帕金森综合征中似乎是PD所特有的，并且在中枢神经系统内对黑质具有选择性。大鼠研究表明，在黑质纹状体多巴胺能细胞群正常的情况下，L-二羟基苯丙氨酸（L-多巴）会导致黑质和纹状体组织中复合物I活性出现25%的可逆性缺陷。对长期高剂量服用L-多巴的PD患者的纹状体组织进行分析，未发现此类缺陷。这些研究及其他研究结果表明，L-多巴治疗不会导致PD纹状体中复合物I缺乏。然而，不能排除在PD黑质的特定环境中，L-多巴可能会加剧已有的复合物I缺陷。
