电子传递抑制剂对线粒体呼吸链细胞色素bc1位点超氧化物生成的影响。
Effect of electron transfer inhibitors on superoxide generation in the cytochrome bc1 site of the mitochondrial respiratory chain.
作者信息
Ksenzenko M, Konstantinov A A, Khomutov G B, Tikhonov A N, Ruuge E K
出版信息
FEBS Lett. 1983 May 2;155(1):19-24. doi: 10.1016/0014-5793(83)80200-2.
Antimycin, 2-nonyl-4-hydroxyquinoline N-oxide and funiculosin induce O.2(-) generation by submitochondrial particles oxidizing succinate, whereas KCN, mucidin, myxothiazol or 2,3-dimercaptopropanol inhibit O.2(-) generation. Thenoyltrifluoroacetone does not induce superoxide production by itself but slightly stimulates the reaction initiated by antimycin. The results indicate that auto-oxidation of unstable ubisemiquinone formed in centre o of the Q-cycle generates most of the O.2(-) radicals in the cytochrome bc1-site of the mitochondrial respiratory chain.
抗霉素、2-壬基-4-羟基喹啉 N-氧化物和绳霉素可通过氧化琥珀酸的亚线粒体颗粒诱导超氧阴离子（O₂⁻）生成，而氰化钾、粘菌素、抗霉素 A 和 2,3-二巯基丙醇则抑制 O₂⁻生成。噻吩甲酰三氟丙酮本身不会诱导超氧化物产生，但会轻微刺激抗霉素引发的反应。结果表明，在 Q 循环中心 o 形成的不稳定泛半醌的自氧化在线粒体呼吸链的细胞色素 bc1 位点产生了大部分 O₂⁻自由基。
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