摘要
为探讨急性胆道感染时肝损害机制,本实验观察了大鼠实验性急性胆道感染对肝细胞线粒体的影响,以及伴随的肝脏储备功能改变。通过对肝细胞线粒体Ca^(2+)含量、溶酶体膜脆性、肝组织过氧化脂质含量、血清OCT,m-GOT酶活性和HPT试验的检测,发现急性胆道感染时肝细胞内存在着线粒体Ca^(2+)超载、溶酶体酶释放、脂质过氧化等,这些均可导致线粒体受累;血清OCT、m-GOT活性升高提示线粒体受损;HPT持续下降,表明线粒体受损同时,肝储备功能进行性受累。
In order to elucidate the mechanism of liver damage due to acute biliary sepsis,the changes of hepatocyte mitochondria were observed during biliary sepsis in the rat.The accompanied liver function changes were also studied.Mitochondrial calcium content,and lysosome fragility of the hepatocytes,lipid peroxide (LPO) level of liver tissue,ornithine carbamoytransferase (OCT),mitochondrial glulamicoxloacetic transaminase (m-GOT),and hepa-toplastin were determined.It was found that there were overloading of calcium in mitochondria,increase of lysosome fragility,and accumulation of LPO in the liver.These events would result in adverse effects on mitochondrial function.The activity of serum OCT and m-GOT was significantly increased,which suggests that mitochondria are seriously damaged since the 2 enzymes mainly come from hepatocyte mitochondria.And the liver reserving function declined progressively.Our study indicates that mitochondrial damage does exist during acute biliary sepsis,which might play an important role in liver damage.
出处
《第三军医大学学报》
CAS
CSCD
北大核心
1991年第6期560-564,共5页
Journal of Third Military Medical University
基金
国家自然科学基金
关键词
胆道病
线粒体
病理学
biliary tract diseases
liver/PA
mitochondria, calcium
lysoso-mes
lipid peroxides
