Saez G, Thornalley P J, Hill H A, Hems R, Bannister J V
Biochim Biophys Acta. 1982 Oct 28;719(1):24-31. doi: 10.1016/0304-4165(82)90302-6.
Autoxidizing cysteine has been shown to produce thiyl and hydroxyl radicals. Hydrogen peroxide increased the yield of both radicals which was inhibited by catalase but stimulated by copper/zinc superoxide dismutase. This effect is due to increased hydrogen peroxide production by copper/zinc superoxide dismutase as a result of superoxide dismutation. The production of superoxide radicals could not be detected probably because of its low reactivity, however, measurement of oxygen uptake and reduction of ferricytochrome c by autoxidizing cysteine clearly implicate the involvement of super oxide radicals. The production of hydroxyl radicals is postulated to proceed through a fenton reaction, however, this may not necessarily be metal ion controlled. Autoxidizing cysteine disrupts the integrity of hepatocytes causing release of glutathione, adenosine triphosphate and lactate dehydrogenase indicating that it is of little use as a therapeutic agent.
已证明自氧化半胱氨酸会产生硫自由基和羟基自由基。过氧化氢会增加这两种自由基的产量,而过氧化氢酶可抑制该产量,铜/锌超氧化物歧化酶则会刺激其产量。这种效应是由于超氧化物歧化产生的铜/锌超氧化物歧化酶使过氧化氢产量增加所致。可能由于超氧自由基的反应活性较低,无法检测到其产生,然而,通过自氧化半胱氨酸对氧摄取和高铁细胞色素c还原的测量清楚地表明超氧自由基参与其中。据推测,羟基自由基的产生是通过芬顿反应进行的,然而,这不一定受金属离子控制。自氧化半胱氨酸会破坏肝细胞的完整性,导致谷胱甘肽、三磷酸腺苷和乳酸脱氢酶释放,这表明它作为治疗剂用途不大。