Zhu Q S, Beattie D S
Department of Biochemistry, West Virginia University School of Medicine, Morgantown 26506.
Biochim Biophys Acta. 1988 Jul 27;934(3):303-13. doi: 10.1016/0005-2728(88)90090-4.
The interaction of the exogenous quinones, duroquinone (DQ) and the decyl analogue of ubiquinone (DB) with the mitochondrial respiratory chain was studied in both wild-type and a ubiquinone-deficient mutant of yeast. DQ can be reduced directly by NADH dehydrogenase, but cannot be reduced by succinate dehydrogenase in the absence of endogenous ubiquinone. The succinate-driven reduction of DQ can be stimulated by DB in a reaction inhibited 50% by antimycin and 70-80% by the combined use of antimycin and myxothiazol, suggesting that electron transfer occurs via the cytochrome b-c1 complex. Both DQ and DB can effectively mediate the reduction of cytochrome b by the primary dehydrogenases through center o, but their ability to mediate the reduction of cytochrome b through center i is negligible. Two reaction sites for ubiquinol seem to be present at center o: one is independent of endogenous Q6 with a high reaction rate and a high Km; the other is affected by endogenous Q6 and has a low reaction rate and a low Km. By contrast, only one ubiquinol reaction site was observed at center i, where DB appears to compete with endogenous Q6. DB can oxidize most of the pre-reduced cytochrome b, while DQ can oxidize only 50%. On the basis of these data, the possible binding patterns of DB on different Q-reaction sites and the requirement for ubiquinone in the continuous oxidation of DQH are discussed.
在野生型酵母和泛醌缺陷型酵母突变体中研究了外源性醌类物质杜醌（DQ）和泛醌癸基类似物（DB）与线粒体呼吸链的相互作用。在没有内源性泛醌的情况下，DQ可被NADH脱氢酶直接还原，但不能被琥珀酸脱氢酶还原。在抗霉素抑制50%、抗霉素和黏噻唑联合使用抑制70 - 80%的反应中，DB可刺激琥珀酸驱动的DQ还原，这表明电子传递通过细胞色素b-c1复合体发生。DQ和DB都能通过中心o有效地介导初级脱氢酶对细胞色素b的还原，但它们通过中心i介导细胞色素b还原的能力可忽略不计。泛醇似乎在中心o存在两个反应位点：一个独立于内源性Q6，反应速率高且Km值高；另一个受内源性Q6影响，反应速率低且Km值低。相比之下，在中心i仅观察到一个泛醇反应位点，在该位点DB似乎与内源性Q6竞争。DB可氧化大部分预还原的细胞色素b，而DQ只能氧化50%。基于这些数据，讨论了DB在不同Q反应位点上可能的结合模式以及DQH持续氧化中对泛醌的需求。
