Hogg N
Biophysics Research Institute, Medical College of Wisconsin, Milwaukee 53226, USA.
Free Radic Biol Med. 1999 Jul;27(1-2):28-33. doi: 10.1016/s0891-5849(99)00029-5.
This study examines the effect of cysteine on the auto-oxidation of homocysteine, a process that has been implicated in the pathologic mechanism of hyperhomocystinemia with respect to arteriosclerosis and vascular disease. It is shown that homocysteine autoxidizes at a much slower rate than cysteine, but that low concentrations of cysteine or cystine dramatically accelerate homocysteine oxidation and increase the rate of homocysteine-dependent oxygen consumption. It is proposed that the major role of homocysteine is to reduce cystine to cysteine, and that cysteine autoxidation is the mechanism by which thiol-dependent oxidative stress occurs.
本研究考察了半胱氨酸对同型半胱氨酸自氧化的影响，这一过程与高同型半胱氨酸血症在动脉粥样硬化和血管疾病方面的病理机制有关。结果表明，同型半胱氨酸的自氧化速度比半胱氨酸慢得多，但低浓度的半胱氨酸或胱氨酸会显著加速同型半胱氨酸的氧化，并提高同型半胱氨酸依赖的耗氧率。研究提出，同型半胱氨酸的主要作用是将胱氨酸还原为半胱氨酸，而半胱氨酸自氧化是硫醇依赖性氧化应激发生的机制。
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