帕金森病患者血小板线粒体呼吸功能的研究  

Studies on the respiratory function of platelet mitochondria in patients with Parkinson's disease

作　　者：马琪林[1] 蔡琰[2] 林其谁[3] 沈崇欣[2] 周孝达[2] 

机构地区：[1]厦门市第一医院神经内科,厦门361003 [2]上海第二医科大学仁济医院神经内科 [3]中国科学院上海生化研究所分子生物学国家重点实验室

出　　处：《临床神经病学杂志》2004年第1期5-7,共3页Journal of Clinical Neurology

基　　金：卫生部科研基金资助项目 (编号 96 2 2 94)

摘　　要：目的　观察帕金森病 (PD)患者的血小板线粒体呼吸功能 ,探讨其与PD发病之间的关系。方法对 35例PD患者提取血小板线粒体后 ,测定其血小板线粒体的呼吸率和呼吸控制率以及复合物Ⅰ、Ⅱ、Ⅲ、Ⅳ的活性变化。结果　PD患者的血小板计数无明显变化 ,但在以谷氨酸 ,苹果酸 +丙酮酸以及琥珀酸为底物时 ,线粒体呼吸状态 3的呼吸率明显下降 ,同时复合物Ⅰ的活性也明显降低 ,而其他复合物活性无明显变化。结论　PD患者的血小板线粒体呼吸功能明显异常 ,可能是PD发病的一个重要机制。Objective To investigate the respiratory function of platelet mitochondria in patients with Parkinson's disease(PD) and explore the assosiation with the pathogenesis of PD.Methods The platelet mitochondria of 35 patients with PD were extracted and the mitochondria respiratory rate and respiratory control rate were measured.Furthermore,the changes of activities of mitochondria complex Ⅰ,Ⅱ,Ⅲ and Ⅳ were observed.Results The platelet counts of patients with PD showed no changes, but the respiratory rates of respiratory state 3 were significantly decreased using the 5 mmol/L glutamate,2.5 mmol/L malate +5 mmol/L pyruvate and 5 mM succinate as substrates. Moreover, the activities of mitochondria complex Ⅰ were obviously reduced and the activites of other mitochondria complex were no changes.Conclusion Patients with PD show exactly abnormal mitochondria respiratory functions, and it might be an important mechanism in the pathogenesis of PD.

关 键 词：帕金森病 血小板 线粒体呼吸功能 发病机制 神经元 氧自由基 

分 类 号：R742.5[医药卫生—神经病学与精神病学]