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通过线粒体孵育液染镉并用N-乙酰半胱氨酸(N-acetylcysteine,NAC)干预研究镉致大鼠肝线粒体损伤的影响。结果显示,随着染镉剂量的增加,MDA含量显著升高(P<0.05),线粒体复合体(Ⅰ+Ⅲ)活性显著降低(P<0.05);线粒体释放细胞色素C(cytochrome C Cyt C)含量显著升高(P<0.05)。且在一定范围内随着CdCl2剂量增加,线粒体复合体(Ⅰ+Ⅲ)活性有降低趋势,MDA含量和Cyt C含量有升高趋势。与单纯染镉组比,NAC预处理组MDA含量和Cyt C含量显著降低,线粒体复合体(Ⅰ+Ⅲ)活性显著升高(P<0.05)。提示镉可以剂量依赖性地诱导大鼠肝线粒体氧化损伤;NAC预处理能有效预防镉所致大鼠肝线粒体氧化损伤。
The mitochondrial damage induced by cadmium in rats was induced by exposure to cadmium by mitochondrial incubation and N-acetylcysteine (NAC) intervention. The results showed that the content of MDA was significantly increased (P <0.05) and the activity of mitochondrial complex (Ⅰ + Ⅲ) was significantly decreased with the increase of cadmium dose (P <0.05). The release of mitochondrial cytochrome C, Content was significantly increased (P <0.05). And within a certain range, the activity of mitochondrial complex (Ⅰ + Ⅲ) decreased and the content of MDA and Cyt C increased with the increase of CdCl2 dose. The content of MDA and Cyt C in NAC pretreatment group was significantly lower than that in pure Cd treatment group (Ⅰ + Ⅲ) (P <0.05). Tip cadmium can dose-dependently induce oxidative damage in rat liver mitochondria; NAC pretreatment can effectively prevent cadmium-induced oxidative damage in rat liver mitochondria.