Mizuno Y, Ohta S, Tanaka M, Takamiya S, Suzuki K, Sato T, Oya H, Ozawa T, Kagawa Y
Department of Neurology, Juntendo University School of Medicine, Tokyo, Japan.
Biochem Biophys Res Commun. 1989 Sep 29;163(3):1450-5. doi: 10.1016/0006-291x(89)91141-8.
Immunoblotting studies on mitochondria prepared from the striata of patients who died of Parkinson's disease were performed using specific antisera against Complexes I, III and IV. In 4 out of 5 patients with Parkinson's disease, the 30-, 25- and 24-kDa subunits of Complex I were moderately to markedly decreased. No clear difference was noted in immunoblotting studies on subunits of Complexes III and IV between the control and Parkinson's disease. Deficiencies in Complex I subunits seem to be one of the most important clues to elucidate pathogenesis of Parkinson's disease.
使用针对复合物I、III和IV的特异性抗血清，对死于帕金森病患者的纹状体中制备的线粒体进行免疫印迹研究。在5例帕金森病患者中，有4例复合物I的30 kDa、25 kDa和24 kDa亚基中度至明显减少。在对照组和帕金森病组之间，复合物III和IV亚基的免疫印迹研究未发现明显差异。复合物I亚基的缺陷似乎是阐明帕金森病发病机制的最重要线索之一。
