帕金森病患者成纤维细胞中丙酮酸氧化脱羧受损

C Mytilineou, P Werner, S Molinari, A Di Rocco, G Cohen, M D Yahr
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引用次数: 95

摘要

帕金森氏症患者脑线粒体复合体I活性的缺乏是否代表了一种包括其他器官或组织的缺陷一直是一些争议的来源。我们通过测量[2-14C]丙酮酸和[1,4- 14c]琥珀酸盐的氧化脱羧,检测了帕金森病患者成纤维细胞的线粒体呼吸。我们报道,与健康对照相比,帕金森患者成纤维细胞中丙酮酸氧化而琥珀酸氧化明显减少。这些观察结果支持了在帕金森病中存在广泛线粒体呼吸缺陷的观点。此外,成纤维细胞培养物是受影响的增殖细胞的来源,可用于呼吸缺陷性质的体外研究和纠正缺陷的药理学干预的测试。
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Impaired oxidative decarboxylation of pyruvate in fibroblasts from patients with Parkinson's disease.

Whether or not a reported deficiency in brain mitochondrial complex I activity in Parkinson's disease represents a defect encompassing other organs or tissues has been a source of some controversy. We have examined mitochondrial respiration in fibroblasts from patients with Parkinson's disease by measuring the oxidative decarboxylation of [2-14C]pyruvate and [1,4-14C]succinate. We report that oxidation of pyruvate but not succinate was significantly reduced in fibroblasts from Parkinson patients when compared to healthy controls. These observations support the view that a widespread deficit in mitochondrial respiration exists in Parkinson's disease. Fibroblast cultures, moreover, are a source of affected proliferating cells, which can be used for in vitro studies of the nature of the respiratory defect and for testing of pharmacological interventions to correct the deficiency.

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