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首页> 外文期刊>Archives of general psychiatry. >Mitochondrial complex I activity and oxidative damage to mitochondrial proteins in the prefrontal cortex of patients with bipolar disorder.
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Mitochondrial complex I activity and oxidative damage to mitochondrial proteins in the prefrontal cortex of patients with bipolar disorder.

机译：线粒体复杂我活动和氧化损伤线粒体中的蛋白质双相患者的前额叶皮层障碍。

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CONTEXT: Accumulating evidence suggests that mitochondrial dysfunction and oxidative stress contribute to the pathogenesis of bipolar disorder and schizophrenia. It remains unclear whether mitochondrial dysfunction, specifically complex I impairment, is associated with increased oxidative damage and, if so, whether this relationship is specific to bipolar disorder. OBJECTIVE: To evaluate whether decreased levels of the electron transport chain complex I subunit NDUFS7 are associated with complex I activity and increased oxidative damage to mitochondrial proteins in the prefrontal cortex of patients with bipolar disorder, schizophrenia, or major depressive disorder. DESIGN: Postmortem prefrontal cortex from patients and controls were assessed using immunoblotting, spectrophotometric, competitive enzyme immunoassay to identify group differences in expression and activity of complex I, and in oxidative damage in mitochondria. SETTING: University of British Columbia, Vancouver, Canada. Patients Forty-five patients with a psychiatric disorder (15 each with bipolar disorder, schizophrenia, and major depressive disorder) and 15 nonpsychiatric control subjects were studied. MAIN OUTCOME MEASURES: Oxidative damage to proteins and mitochondrial complex I activity. RESULTS: Levels of NDUFS7 and complex I activity were decreased significantly in patients with bipolar disorder but were unchanged in those with depression and schizophrenia compared with controls. Protein oxidation, as measured by protein carbonylation, was increased significantly in the bipolar group but not in the depressed or schizophrenic groups compared with controls. We observed increased levels of 3-nitrotyrosine in the bipolar disorder and schizophrenia groups. CONCLUSIONS: Impairment of complex I may be associated with increased protein oxidation and nitration in the prefrontal cortex of patients with bipolar disorder. Therefore, complex I activity and mitochondrial dysfunction may be potential therapeutic targets for bipolar disorder.
机译：背景:越来越多的证据表明线粒体功能障碍和氧化应激双相情感障碍的发病机制障碍和精神分裂症。线粒体功能障碍,是否明确复杂的我损伤,与增加氧化损伤,如果是这样,是否这种关系是特定于双相障碍。电子传递链的水平下降复杂的我亚基NDUFS7是相关的复杂的活动,增加氧化损伤线粒体蛋白质在前额双相情感障碍患者的皮层,精神分裂症或重度抑郁症。设计:后期前额叶皮层病人和控制评估使用免疫印迹、光谱光度测量的竞争力酶免疫分析法来确定组的差异表达和活动的复杂的我,在线粒体氧化损伤。温哥华英属哥伦比亚大学,加拿大。每个双相精神障碍(15障碍、精神分裂症、抑郁15非精神障碍)和对照组进行了研究。蛋白质和线粒体损伤复杂的我活动。活动在患者明显减少在那些患有双相情感障碍,但不变与抑郁和精神分裂症相比控制。蛋白质羰基化,增加双组但不显著抑郁或精神分裂症组相比控制。在双相情感障碍和3-nitrotyrosine精神分裂症组。复杂的我可能会增加前额叶的蛋白质氧化和硝化双相情感障碍患者的皮层。因此,复杂的我活动和线粒体功能障碍可能是潜在的治疗靶点双相情感障碍。

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