Kolesova G M, Kapitanova N G, Iaguzhinskiĭ L S
Biokhimiia. 1987 May;52(5):715-9.
It was shown that hydrophilic benzo- and naphthoquinones stimulate the cyanide-resistant respiration in liver and muscle mitochondria when succinate or NADH and glutamate or malate are used as oxidation substrates. The substrate-dependent oxygen uptake in the presence of cyanide is initiated by menadione, vicasol, 1.2-naphthoquinone, coenzyme Q0 and duroquinone. Rotenone and antimycin A do not inhibit the cyanide-resistant respiration. Oxidation of glutamate and malate in the course of CN-resistant respiration is inhibited by ortho- and bathophenanthroline and p-chloromercurybenzoate, whereas succinate oxidation by tenoyltrifluoroacetone, carboxin and pentachlorophenol. Superoxide dismutase, Cu2+ and catalase inhibit the CN-resistant respiration in the presence of quinones. Addition of catalase to the experimental cell causes O2 release.
结果表明，当使用琥珀酸或NADH以及谷氨酸或苹果酸作为氧化底物时，亲水性苯醌和萘醌会刺激肝脏和肌肉线粒体中的抗氰呼吸。在氰化物存在的情况下，底物依赖性氧气摄取由甲萘醌、维生素K4、1,2-萘醌、辅酶Q0和杜醌引发。鱼藤酮和抗霉素A不抑制抗氰呼吸。在抗氰呼吸过程中，谷氨酸和苹果酸的氧化受到邻菲罗啉和bathophenanthroline以及对氯汞苯甲酸的抑制，而琥珀酸氧化则受到十酰三氟丙酮、萎锈灵和五氯苯酚的抑制。超氧化物歧化酶、Cu2+和过氧化氢酶在醌存在的情况下会抑制抗氰呼吸。向实验细胞中添加过氧化氢酶会导致氧气释放。
