Degli Esposti M, Tsai A L, Palmer G, Lenaz G
Eur J Biochem. 1986 Nov 3;160(3):547-55. doi: 10.1111/j.1432-1033.1986.tb10073.x.
We have investigated the oxidation of the reduced ubiquinol:cytochrome c reductase (bc1 complex) isolated from beef heart mitochondria. The oxidation of cytochrome c1 by both potassium ferricyanide and cytochrome c in the ascorbate-reduced bc1 complex is not a first-order process. This is taken as evidence that cytochrome c1 is in rapid equilibrium with the Rieske iron-sulphur center. Among the several inhibitors tested, only 5-n-undecyl-6-hydroxy-4,7-dioxobenzothiazole and stigmatellin are seen to affect this redox equilibrium between the high-potential centers of the beef heart bc1 complex. The oxidation of cytochrome b by cytochrome c in both the succinate-reduced and the fully reduced bc1 complex is blocked by all the inhibitors tested. This inhibition occurs simultaneously with an acceleration in the oxidation of cytochrome c1, even after extraction of the endogenous ubiquinone which is present in the bc1 preparation. Almost complete extraction of ubiquinone from the bc1 complex has no effect upon the rapid phase of cytochrome b oxidation, nor does it alter the inhibition of cytochrome b oxidation by the various inhibitors. The oxidation of cytochrome b by exogenous ubiquinones is stimulated by myxothiazol and partially inhibited by antimycin. However, the addition of both these inhibitors together completely blocks the oxidation of cytochrome b by quinones. In contrast, the simultaneous addition of antimycin and myxothiazol has no such synergistic effect upon the oxidation of cytochrome b by cytochrome c. Our data show that intramolecular electron transfer from cytochrome(s) b to the Rieske iron-sulphur center can take place in the bc1 complex without involvement of endogenous ubiquinone-10. This electron pathway is sensitive to all the inhibitors of the enzyme.
细胞色素c还原酶（bc1复合物）的氧化过程。在抗坏血酸还原的bc1复合物中，铁氰化钾和细胞色素c对细胞色素c1的氧化均不是一级反应过程。这被视为细胞色素c1与 Rieske 铁硫中心处于快速平衡的证据。在测试的几种抑制剂中，只有5 - n - 十一烷基 - 6 - 羟基 - 4,7 - 二氧代苯并噻唑和鱼藤酮能影响牛心bc1复合物高电位中心之间的这种氧化还原平衡。在琥珀酸还原和完全还原的bc1复合物中，细胞色素c对细胞色素b的氧化被所有测试的抑制剂阻断。即使在提取了bc1制剂中存在的内源性泛醌后，这种抑制作用仍与细胞色素c1氧化加速同时发生。从bc1复合物中几乎完全提取泛醌对细胞色素b氧化的快速阶段没有影响，也不会改变各种抑制剂对细胞色素b氧化的抑制作用。粘噻唑刺激外源性泛醌对细胞色素b的氧化，抗霉素部分抑制该反应。然而，同时添加这两种抑制剂会完全阻断醌对细胞色素b的氧化。相比之下，同时添加抗霉素和粘噻唑对细胞色素c氧化细胞色素b没有这种协同作用。我们的数据表明，在bc1复合物中，细胞色素b到 Rieske 铁硫中心的分子内电子转移可以在不涉及内源性泛醌 - 10的情况下发生。这条电子途径对该酶的所有抑制剂敏感。
