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
出处
《中风与神经疾病杂志》
CAS
CSCD
北大核心
1998年第6期345-347,共3页
Journal of Apoplexy and Nervous Diseases
