Role of glutathione on acrolein-induced cytotoxicity and mutagenicity in Escherichia coli
Role of glutathione on acrolein-induced cytotoxicity and mutagenicity in Escherichia coli
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DOI：
10.1016/s1383-5718(99)00052-2
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发表时间：
1999-06-07
影响因子：
1.9
通讯作者：
Yamamoto, K
中科院分区：
文献类型：
--
作者：
Nunoshiba, T;Yamamoto, K
还原型谷胱甘肽(GSH)是一种广为人知的抗氧化剂，但很少有报道表明谷胱甘肽对保护大肠杆菌细胞免受氧化损伤的致命影响有贡献。在这里，我们报告了谷胱甘肽的耗竭导致大肠杆菌对丙烯醛的超敏反应，丙烯醛是结构最简单的α，β-不饱和醛，源于脂质过氧化降解，并且GSH在体外可以与丙烯醛发生化学反应，从而降低其毒性。我们进一步证明，丙烯醛使谷胱甘肽氧化还原酶失活，随后谷胱甘肽耗尽，这可能是丙烯醛的毒性作用的一部分。这些结果表明，GSH有助于细胞防御毒性效应。(C)1999 Elsevier Science B.V.保留所有权利。
The reduced form of glutathione (GSH) is a well-known antioxidant, while there have been few reports indicating the contribution of glutathione to protection of Escherichia coli cells from the lethal effect of oxidative damage. Here, we report that depletion of glutathione causes hypersensitivity of E. coli to acrolein, the structurally simplest alpha, beta-unsaturated aldehyde derived from lipid peroxide-degradation, and that GSH can chemically react with acrolein in vitro thus reducing its toxicity. We further demonstrated that acrolein inactivates glutathione oxidoreductase followed by depletion of glutathione, probably as a part of the toxic effect of acrolein. These results suggested that GSH contributes to cellular defense against the toxic effects. (C) 1999 Elsevier Science B.V. All rights reserved.