Sugiyama M, Tsuzuki K
Department of Medical Biochemistry, Kurume University School of Medicine, Japan.
FEBS Lett. 1994 Mar 21;341(2-3):273-6. doi: 10.1016/0014-5793(94)80471-0.
Incubation of Chinese hamster V-79 cells with either buthionine sulfoximine (BSO) or diethylmaleate (DEM) prior to exposure to Na2CrO4 resulted in a depletion of GSH. ESR study shows that the depletion of GSH by BSO caused an increase in the cellular level of Cr(V) intermediate without affecting the level of Cr(III) complex, whereas the levels of Cr(V) and (III) were both suppressed by the depletion of GSH by DEM. GSH depletion by DEM decreased cellular uptake of chromate more than that by BSO. Glutathione reductase activity in cells, which is capable of reducing Cr(VI), was unaffected by BSO, however a strong inhibition was observed in cells treated with DEM, indicating that DEM affects not only GSH levels but also Cr(VI)-reducing enzyme activity. Thus, the depletion of GSH in cells increases Cr(V) formation, based upon the effect of BSO. The role of intracellular GSH in Cr(VI) reduction is discussed.
在将中国仓鼠V - 79细胞暴露于铬酸钠之前,先用丁硫氨酸亚砜胺(BSO)或马来酸二乙酯(DEM)进行孵育,会导致谷胱甘肽(GSH)耗竭。电子自旋共振(ESR)研究表明,BSO导致的GSH耗竭会使细胞内Cr(V)中间体水平升高,而不影响Cr(III)络合物的水平,而DEM导致的GSH耗竭则会抑制Cr(V)和Cr(III)的水平。与BSO相比,DEM导致的GSH耗竭使细胞对铬酸盐的摄取减少得更多。细胞中能够还原Cr(VI)的谷胱甘肽还原酶活性不受BSO影响,但在用DEM处理的细胞中观察到强烈抑制,这表明DEM不仅影响GSH水平,还影响Cr(VI)还原酶活性。因此,基于BSO的作用,细胞内GSH的耗竭会增加Cr(V)的形成。本文讨论了细胞内GSH在Cr(VI)还原中的作用。