Bowyer J R, Trumpower B L
J Biol Chem. 1981 Mar 10;256(5):2245-51.
Antimycin, a specific and highly potent inhibitor of electron transfer in the cytochrome b-c1 segment of the mitochondrial respiratory chain, does not inhibit reduction of cytochrome c1 by succinate in isolated succinate-cytochrome c reductase complex under conditions where the respiratory chain complex undergoes one oxidation-reduction turnover. If a slight molar excess of cytochrome c is added to the isolated reductase complex in the presence of antimycin, there is rapid reduction of one equivalent of c type cytochrome by succinate, after which reduction of the remaining c type cytochrome is inhibited. Antimycin fully inhibits succinate-cytochrome c reductase activity of isolated succinate-cytochrome c reductase complex in which the b-c1 complex undergoes multiple turnovers in a catalytic fashion. In addition, when antimycin is added to isolated reductase complex in the presence of cytochrome c plus cytochrome c oxidase, the inhibitor causes a "crossover" in the steady state level of reduction of the cytochromes b and c1 comparable to this classical effect in mitochondria. On the basis of these results, it is suggested that linear schemes of electron transfer are not adequate to account for the site of antimycin inhibition and the mechanism of electron transfer in the cytochrome b-c1 segment of the respiratory chain. The effects of antimycin are consistent with cyclic electron transfer mechanisms such as the protonmotive Q cycle.
抗霉素是线粒体呼吸链细胞色素b-c1段电子传递的一种特异性高效抑制剂，在呼吸链复合体经历一次氧化还原周转的条件下，它不会抑制分离的琥珀酸-细胞色素c还原酶复合体中琥珀酸对细胞色素c1的还原作用。如果在抗霉素存在的情况下，向分离的还原酶复合体中加入略微摩尔过量的细胞色素c，琥珀酸会迅速将一当量的c型细胞色素还原，之后其余c型细胞色素的还原受到抑制。抗霉素能完全抑制分离的琥珀酸-细胞色素c还原酶复合体的琥珀酸-细胞色素c还原酶活性，其中b-c1复合体以催化方式进行多次周转。此外，当在细胞色素c加细胞色素c氧化酶存在的情况下，将抗霉素加入到分离的还原酶复合体中时，该抑制剂会导致细胞色素b和c1还原的稳态水平出现“交叉”，这与线粒体中的这种经典效应类似。基于这些结果，有人提出，电子传递的线性模式不足以解释抗霉素的抑制位点以及呼吸链细胞色素b-c1段的电子传递机制。抗霉素的作用与循环电子传递机制如质子动力Q循环是一致的。
