Shi X L, Dalal N S
Department of Chemistry, West Virginia University Morgantown 26506.
Biochem Biophys Res Commun. 1989 Aug 30;163(1):627-34. doi: 10.1016/0006-291x(89)92183-9.
Electron spin resonance measurements provide evidence for the formation of long-lived Cr(V) intermediates in the reduction of Cr(VI) by glutathione reductase in the presence of NADPH and for the hydroxyl radical formation during the glutathione reductase catalyzed reduction of Cr(VI). Hydrogen peroxide suppresses Cr(V) and enhances the formation of hydroxyl radicals. Thus Cr(V) intermediates catalyze generation of hydroxyl radicals from hydrogen peroxide through a Fenton-like reaction. Thus the mechanism of Cr(VI) toxicity might involve the interaction between macromolecules and the hydroxyl radicals.
电子自旋共振测量结果表明，在存在烟酰胺腺嘌呤二核苷酸磷酸（NADPH）的情况下，谷胱甘肽还原酶将六价铬（Cr(VI)）还原过程中会形成长寿命的五价铬（Cr(V)）中间体，并且在谷胱甘肽还原酶催化的六价铬（Cr(VI)）还原过程中会形成羟基自由基。过氧化氢会抑制五价铬（Cr(V)）的生成并增强羟基自由基的形成。因此，五价铬（Cr(V)）中间体通过类似芬顿反应的过程催化过氧化氢生成羟基自由基。所以，六价铬（Cr(VI)）毒性的机制可能涉及大分子与羟基自由基之间的相互作用。
