泛醌对阿霉素线粒体氧化磷酸化抑制作用的影响。
Influence of ubiquinone on the inhibitory effect of adriamycin on mitochondrial oxidative phosphorylation.
作者信息
Muhammed H, Kurup C K
出版信息
Biochem J. 1984 Jan 15;217(2):493-8. doi: 10.1042/bj2170493.
The inhibition of succinate oxidation in both heart and liver mitochondria by the cardiotoxic anticancer antibiotic adriamycin in vitro was reversed to a large extent by exogenous ubiquinone-45. Inhibition of the oxidation of NAD+-linked substrates in heart and liver mitochondria responded differently to ubiquinone, the inhibition being reversed only in liver organelles. Administration of adriamycin inhibited oxidative phosphorylation in rat heart, kidney and liver mitochondria, the inhibition being highest in the heart organelles (about 50% for both NAD+-linked substrates and succinate). Exogenous addition of ubiquinone to mitochondria isolated from drug-treated animals did not reverse the inhibition. Administration of ubiquinone along with adriamycin did not change effectively the pattern of drug-mediated decrease in oxidative activity of the organelles, particularly in the heart.
心脏毒性抗癌抗生素阿霉素在体外对心脏和肝脏线粒体中琥珀酸氧化的抑制作用，在很大程度上可被外源性泛醌-45逆转。心脏和肝脏线粒体中与NAD⁺相关底物氧化的抑制对泛醌的反应不同，仅在肝脏细胞器中抑制作用被逆转。给予阿霉素会抑制大鼠心脏、肾脏和肝脏线粒体中的氧化磷酸化，在心脏细胞器中的抑制作用最强（对于与NAD⁺相关底物和琥珀酸均约为50%）。向从经药物处理动物分离的线粒体中外源性添加泛醌并不能逆转抑制作用。与阿霉素一起给予泛醌并不能有效改变药物介导的细胞器氧化活性降低模式，尤其是在心脏中。
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