Shi X L, Sun X Y, Dalal N S
Department of Chemistry, West Virginia University Morgantown, WV 26506.
FEBS Lett. 1990 Oct 1;271(1-2):185-8. doi: 10.1016/0014-5793(90)80402-5.
The in vivo toxicity of vanadium(V) has been found to correlate with the depletion of cellular glutathione and related non-protein thiols. With a view to understanding the mechanism for this observation, we have investigated the oxidation of glutathione, cysteine N-acetylcysteine and penicillamine by vanadium(V), using electron spin resonance (ESR) and ESR spin trapping methodology. The spin trap used was 5,5-dimethyl-1-pyrroline 1-oxide (DMPO). It is found that the oxidation of these thiols by vanadium(V) generates the corresponding thiyl radicals and vanadium- (IV) complexes. The results suggest that free radical reactions play a significant role in the depletion of cellular thiols by vanadium(V) and hence in vanadium(V) toxicity.
已发现钒（V）的体内毒性与细胞内谷胱甘肽及相关非蛋白质硫醇的消耗有关。为了理解这一观察结果的机制，我们使用电子自旋共振（ESR）和ESR自旋捕获方法研究了钒（V）对谷胱甘肽、半胱氨酸、N - 乙酰半胱氨酸和青霉胺的氧化作用。所使用的自旋捕获剂是5,5 - 二甲基 - 1 - 吡咯啉 - N - 氧化物（DMPO）。发现钒（V）对这些硫醇的氧化会产生相应的硫自由基和钒（IV）配合物。结果表明，自由基反应在钒（V）导致细胞硫醇消耗中起重要作用，因此在钒（V）毒性中也起重要作用。
