Ostrovsky D N
A. N. Bach Institute of Biochemistry, U.S.S.R. Academy of Sciences, Moscow.
Biochem J. 1990 Mar 1;266(2):481-6. doi: 10.1042/bj2660481.
Endogenous coupled respiration of Micrococcus luteus protoplasts showed a relatively high resistance to low concentrations of KCN, 2-nonyl-4-hydroxyquinoline N-oxide (NQNO) and dicyclohexylcarbodi-imide (DCCD) when the inhibitors were applied individually. In the presence of both KCN and NQNO (or DCCD), O2 uptake was strongly inhibited. The proteolysis of external membrane proteins of protoplasts also induced the high sensitivity of endogenous coupled respiration to low KCN. The effects of NQNO, DCCD and proteolysis were explained by the inhibition of an alternative respiratory system when reducing equivalents passed preferentially down the KCN-sensitive cytochrome oxidase. Uncoupling of the cell membrane increased the electron flow via the cytochrome oxidase-containing respiratory branch. It is suggested that the energy state of cells could control the electron-flow distribution between two branches, and quinones of different levels of reduction could be involved in the mechanism of respiratory branching.
藤黄微球菌原生质体的内源性偶联呼吸在单独应用抑制剂时，对低浓度的氰化钾（KCN）、2-壬基-4-羟基喹啉N-氧化物（NQNO）和二环己基碳二亚胺（DCCD）表现出相对较高的抗性。当同时存在KCN和NQNO（或DCCD）时，氧气摄取受到强烈抑制。原生质体外膜蛋白的蛋白水解也诱导了内源性偶联呼吸对低浓度KCN的高敏感性。当还原当量优先通过对KCN敏感的细胞色素氧化酶传递时，NQNO、DCCD和蛋白水解的作用可以通过对替代呼吸系统的抑制来解释。细胞膜的解偶联增加了通过含细胞色素氧化酶的呼吸支路的电子流。有人提出，细胞的能量状态可以控制两个支路之间的电子流分布，不同还原水平的醌可能参与呼吸分支机制。
