二氧化锗诱导的线粒体肌病动物模型的发病机制的研究  

The pathogenesis of experimental model of mitochondrial myopathy induced by germanium dioxide

作　　者：李晓东[1] 高枫[1] 陈清棠[1] 

机构地区：[1]北京医科大学第一医院神经内科

出　　处：《中风与神经疾病杂志》1998年第6期345-347,共3页Journal of Apoplexy and Nervous Diseases

摘　　要：目的建立线粒体肌病的动物模型，以探讨线粒体肌病的发病机制。方法利用二氧化锗喂养Ｗｉｓｔａｒ大鼠２４周，进行肌肉病理检查，测定生化功能及线粒体ＤＮＡ含量。结果线粒体肌病动物模型被建立，其细胞内自由基含量增多，线粒体ＤＮＡ拷贝数明显减少。结论可能有部分线粒体肌病由环境毒素引起。Objective To the study was to build up an animal model of mitochondrial myopathy in order to analyse the pathogenesis of the disease Method The skeletal muscles from Wistar rats treated with germanium dioxide for 24 weeks were analysed by histopathologic and electro microscopic studies A quantitative analysis was carried out in mitochondrial DNAs of these samples The biological function of the model was determined Results An animal model of mitochondrial myopathy was builded up,in which oxygen free radicals were increased and mitochondrial DNA copies were decreased contrasted with controls Conclusion It suggested that enviromental toxin may be play a role in the pathogenesis of mitochondrial myopathy The increase of oxygen free radicals is a important link causing the disease

关 键 词：线粒体肌病 动物模型 二氧化锗 诱导 

分 类 号：R746.02[医药卫生—神经病学与精神病学]