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大肠杆菌的核酸内切酶IV由百草枯诱导产生。

Endonuclease IV of Escherichia coli is induced by paraquat.

作者信息

Chan E, Weiss B

出版信息

Proc Natl Acad Sci U S A. 1987 May;84(10):3189-93. doi: 10.1073/pnas.84.10.3189.

Abstract

The addition of paraquat (methyl viologen) to a growing culture of Escherichia coli K-12 led within 1 hr to a 10- to 20-fold increase in the level of endonuclease IV, a DNase for apurinic/apyrimidinic sites. The induction was blocked by chloramphenicol. Increases of 3-fold or more were also seen with plumbagin, menadione, and phenazine methosulfate. H2O2 produced no more than a 2-fold increase in endonuclease IV activity. The following agents had no significant effect: streptonigrin, nitrofurantoin, tert-butyl hydroperoxide, gamma rays, 260-nm UV radiation, methyl methanesulfonate, mitomycin C, and ascorbate. Paraquat, plumbagin, menadione, and phenazine methosulfate are known to generate superoxide radical anions via redox cycling in vivo. A mutant lacking superoxide dismutase was unusually sensitive to induction by paraquat. In addition, endonuclease IV could be induced by merely growing the mutant in pure O2. The levels of endonuclease IV in uninduced or paraquat-treated cells were unaffected by mutations of oxyR, a H2O2-inducible gene that governs an oxidative-stress regulon. The results indicate that endonuclease IV is an inducible DNA-repair enzyme and that its induction can be mediated via the production of superoxide radicals.

摘要

在大肠杆菌K-12的生长培养物中添加百草枯(甲基紫精),1小时内即可使内切核酸酶IV(一种作用于无嘌呤/无嘧啶位点的DNA酶)的水平增加10至20倍。氯霉素可阻断这种诱导作用。此外,白花丹醌、甲萘醌和吩嗪硫酸甲酯也能使该酶水平增加3倍或更多。过氧化氢使内切核酸酶IV活性增加不超过2倍。以下试剂无显著影响:链黑菌素、呋喃妥因、叔丁基过氧化氢、γ射线、260纳米紫外线辐射、甲基磺酸甲酯、丝裂霉素C和抗坏血酸。已知百草枯、白花丹醌、甲萘醌和吩嗪硫酸甲酯可通过体内氧化还原循环产生超氧阴离子自由基。一种缺乏超氧化物歧化酶的突变体对百草枯诱导异常敏感。此外,仅将该突变体在纯氧中培养即可诱导产生内切核酸酶IV。内切核酸酶IV在未诱导或经百草枯处理的细胞中的水平不受oxyR(一个控制氧化应激调节子的H2O2诱导基因)突变的影响。结果表明,内切核酸酶IV是一种可诱导的DNA修复酶,其诱导可通过超氧自由基的产生介导。

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