Pittsburgh Institute for Neurodegenerative Diseases, 3501 Fifth Avenue, 7038 Biomedical Science Tower 3, Pittsburgh, PA 15261, USA.
J Bioenerg Biomembr. 2009 Dec;41(6):469-72. doi: 10.1007/s10863-009-9257-z.
The etiology of sporadic Parkinson's disease (PD) is unknown, although mitochondrial dysfunction and oxidative stress have been implicated in the mechanisms associated with PD pathogenesis. Dopamine (DA) neurons of the substantia nigra pars compacta have been shown to degenerate to a greater extent in PD than other neurons suggesting the possibility that DA itself may be contributing to the neurodegenerative process. This review discusses our work on the effects of DA oxidation and reactive DA quinones on mitochondrial function and protein modification and the potential for exacerbating toxicity associated with mitochondrial dysfunction in PD.
散发性帕金森病（PD）的病因尚不清楚，尽管线粒体功能障碍和氧化应激与 PD 发病机制相关的机制有关。已经表明，与其他神经元相比，黑质致密部的多巴胺（DA）神经元在 PD 中更明显地退化，这表明 DA 本身可能有助于神经退行性过程。这篇综述讨论了我们关于 DA 氧化和反应性 DA 醌对线粒体功能和蛋白质修饰的影响，以及它们可能加剧与 PD 中线粒体功能障碍相关的毒性的潜力。
