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STUDIES ON CHROMATED ERYTHROCYTES. EFFECT OF SODIUM CHROMATE ON ERYTHROCYTE GLUTATHIONE REDUCTASE.铬化红细胞的研究。铬酸钠对红细胞谷胱甘肽还原酶的影响。
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Chromium(VI)-induced DNA lesions and chromium distribution in rat kidney, liver, and lung.六价铬诱导的大鼠肾脏、肝脏和肺中的DNA损伤及铬分布。
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In vitro effects of N-acetylcysteine on the mutagenicity of direct-acting compounds and procarcinogens.N-乙酰半胱氨酸对直接作用化合物和前致癌物致突变性的体外效应。
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Vitamin E protects against methyl ethyl ketone peroxide-induced peroxidative damage to rat brain DNA.维生素E可防止过氧化甲乙酮诱导的对大鼠脑DNA的过氧化损伤。
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维生素对六价铬诱导损伤的影响。

Effects of vitamins on chromium(VI)-induced damage.

作者信息

Sugiyama M

机构信息

Department of Medical Biochemistry, Kurume University School of Medicine, Japan.

出版信息

Environ Health Perspect. 1991 May;92:63-70. doi: 10.1289/ehp.919263.

DOI:10.1289/ehp.919263
PMID:1935852
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1519399/
Abstract

The effects of vitamin E and vitamin B2 on DNA damage and cellular reduction of chromium(VI) were investigated using Chinese hamster V-79 cells. Pretreatment with alpha-tocopherol succinate (vitamin E) resulted in a decrease of DNA single-strand breaks produced by Na2CrO4, while similar treatment with riboflavin (vitamin B2) enhanced levels of DNA breaks. In contrast, levels of DNA-protein crosslinks induced by Na2CrO4 were unaffected by these vitamins. Electron spin resonance (ESR) studies showed that incubation of cells with Na2CrO4 resulted in the formation of both chromium(V) and chromium(III) complexes, and cellular pretreatment with vitamin E reduced the level of the chromium(V) complex, whereas pretreatment with vitamin B2 enhanced the level of this intermediate. However, the levels of chromium(III) were unchanged by these vitamins. The uptake of chromate was not affected by vitamin E or vitamin B2, nor were the levels of glutathione or glutathione reductase activity, which are both capable of reducing chromate. ESR studies demonstrated that a chromium(V) species was formed by the reaction of Na2CrO4 with vitamin B2 and that vitamin B2 enhanced the formation of hydroxyl radicals during the reaction of Na2CrO4 and hydrogen peroxide. Treatment cells with Na2CrO4 resulted in a decrease of glutathione reductase activity, and pretreatment with vitamin E restored the enzyme activity suppressed by this metal. However, pretreatment with vitamin B2 enhanced the inhibition of this enzyme by Na2CrO4. Using a colony-forming assay, pretreatment with vitamin E dramatically decreased the cytotoxicity of Na2CrO4, while pretreatment with vitamin B2 was found to result in only a decrease of cell lethality of this metal.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

利用中国仓鼠V - 79细胞研究了维生素E和维生素B2对DNA损伤及六价铬细胞还原的影响。用琥珀酸生育酚(维生素E)预处理可使铬酸钠产生的DNA单链断裂减少,而用核黄素(维生素B2)进行类似处理则会提高DNA断裂水平。相比之下,铬酸钠诱导的DNA - 蛋白质交联水平不受这些维生素的影响。电子自旋共振(ESR)研究表明,细胞与铬酸钠孵育会导致形成铬(V)和铬(III)复合物,用维生素E对细胞进行预处理可降低铬(V)复合物的水平,而用维生素B2预处理则会提高这种中间体的水平。然而,这些维生素对铬(III)的水平没有影响。铬酸盐的摄取不受维生素E或维生素B2的影响,谷胱甘肽水平或谷胱甘肽还原酶活性也不受影响,这两者都能够还原铬酸盐。ESR研究表明,铬酸钠与维生素B2反应会形成铬(V)物种,并且维生素B2会在铬酸钠与过氧化氢反应过程中增强羟基自由基的形成。用铬酸钠处理细胞会导致谷胱甘肽还原酶活性降低,用维生素E预处理可恢复被这种金属抑制的酶活性。然而,用维生素B2预处理会增强铬酸钠对这种酶的抑制作用。使用集落形成试验,用维生素E预处理可显著降低铬酸钠的细胞毒性,而用维生素B2预处理仅会导致这种金属的细胞致死率降低。(摘要截短于250字)