Medical Toxicology Centre, Wolfson Unit, Newcastle University, Claremont Place, Newcastle upon Tyne NE2 4AA, UK.
Parkinsons Dis. 2011 Mar 15;2011:716871. doi: 10.4061/2011/716871.
Parkinson's disease (PD) is a progressive, neurodegenerative condition that has increasingly been linked with mitochondrial dysfunction and inhibition of the electron transport chain. This inhibition leads to the generation of reactive oxygen species and depletion of cellular energy levels, which can consequently cause cellular damage and death mediated by oxidative stress and excitotoxicity. A number of genes that have been shown to have links with inherited forms of PD encode mitochondrial proteins or proteins implicated in mitochondrial dysfunction, supporting the central involvement of mitochondria in PD. This involvement is corroborated by reports that environmental toxins that inhibit the mitochondrial respiratory chain have been shown to be associated with PD. This paper aims to illustrate the considerable body of evidence linking mitochondrial dysfunction with neuronal cell death in the substantia nigra pars compacta (SNpc) of PD patients and to highlight the important need for further research in this area.
帕金森病(PD)是一种进行性神经退行性疾病,越来越多地与线粒体功能障碍和电子传递链抑制有关。这种抑制导致活性氧的产生和细胞能量水平的消耗,从而导致氧化应激和兴奋毒性介导的细胞损伤和死亡。已经发现一些与遗传性 PD 形式有关的基因编码线粒体蛋白或与线粒体功能障碍有关的蛋白质,这支持了线粒体在 PD 中的核心作用。这一作用得到了以下报告的证实:已经表明,抑制线粒体呼吸链的环境毒素与 PD 有关。本文旨在说明大量证据表明线粒体功能障碍与 PD 患者黑质致密部(SNpc)神经元细胞死亡有关,并强调在这一领域进一步研究的重要性。