论文部分内容阅读
我们已报道过黄腐酸(Fulvic acid,FA)可引发大鼠肝细胞产生活性氧自由基,并导致生物体的氧化性损伤.但是,作为一种外源性物质,黄腐酸在细胞内怎样转化,通过何种机制引发肝细胞产生内源性活性氧物质,尚不清楚.一般认为,外源性物质多是通过肝细胞内氧化-还原酶体系进行生物转化,进而产生活性氧物质.而此类酶体系多存在于线粒体或微粒体中,本文以大鼠肝细胞线粒体和微粒体为研究对象,研究了黄腐酸与微粒体、线粒体的相互作用过程,并探讨了产生活性氧的可能机制.
We have reported that fulvic acid (FA) can induce reactive oxygen species in rat hepatocytes and result in oxidative damage to the organism. However, fulvic acid, as an exogenous substance, It is not clear what mechanism to induce endogenous reactive oxygen species in liver cells, and it is generally believed that exogenous substances are mostly biologically converted by the intracellular oxidoreductase system in liver cells to produce reactive oxygen species. However, these enzyme systems exist in mitochondria or microsomes. In this paper, the mitochondria and microsomes of rat hepatocytes were studied to study the interaction between fulvic acid and microsomes and mitochondria, Possible mechanism.