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大肠杆菌中ahpC、katG和katE基因的转录受多胺调控:多胺缺陷型突变体对H2O2诱导的氧化损伤敏感。

Transcription of ahpC, katG, and katE genes in Escherichia coli is regulated by polyamines: polyamine-deficient mutant sensitive to H2O2-induced oxidative damage.

作者信息

Jung Il Lae, Kim In Gyu

机构信息

Department of Radiation Biology, Environmental Radiation Research Group, Korea Atomic Energy Research Institute, P.O. Box 105, 305-600, Yusong Taejon, Republic of Korea.

出版信息

Biochem Biophys Res Commun. 2003 Feb 21;301(4):915-22. doi: 10.1016/s0006-291x(03)00064-0.

Abstract

Polyamines (putrescine and spermidine) are present in almost all living organisms and participate in numerous cellular processes. In this study, we report the protective roles of polyamines against hydrogen peroxide (H2O2)-induced oxidative stress. All of ahpC, katG, and katE genes, known to participate in the antioxidant defense mechanism against H2O2-induced stress in Escherichia coli, failed to induce in the absence of polyamines during normal aerobic growth. The induction of both oxyR and rpoS gene expression, whose products are essential to induce ahpC, katG, and katE genes, was also absolutely dependent on polyamines. Polyamine-deficient E. coli mutant has increased susceptibility to exogenous H2O2, and this cell cytotoxicity was relieved to a wild-type level by addition of putrescine or spermidine (1mM), which restored the transcriptional induction of ahpC, katG, and katE genes. H2O2-removing capacity was measured in the mutant, showing a significantly low H2O2-removing capacity compared to the wild type when polyamines were not present. We concluded that the increased susceptibility of the polyamine-deficient E. coli mutant to H2O2 treatment resulted from an intracellular low level of H2O2-removing capacity through the failure of their regulons, ahpC, katG, and katE induction, as well as the failure of oxyR and rpoS induction.

摘要

多胺(腐胺和亚精胺)存在于几乎所有的生物体中,并参与众多细胞过程。在本研究中,我们报道了多胺对过氧化氢(H₂O₂)诱导的氧化应激的保护作用。在大肠杆菌正常需氧生长过程中,所有已知参与对抗H₂O₂诱导应激的抗氧化防御机制的ahpC、katG和katE基因,在缺乏多胺的情况下均无法被诱导。oxyR和rpoS基因表达的诱导,其产物对于诱导ahpC、katG和katE基因至关重要,也绝对依赖于多胺。缺乏多胺的大肠杆菌突变体对外源H₂O₂的敏感性增加,通过添加腐胺或亚精胺(1 mM)可将这种细胞毒性缓解至野生型水平,这恢复了ahpC、katG和katE基因的转录诱导。在突变体中测量了H₂O₂清除能力,结果表明在不存在多胺时,与野生型相比H₂O₂清除能力显著较低。我们得出结论,缺乏多胺的大肠杆菌突变体对H₂O₂处理敏感性增加是由于其调节子ahpC、katG和katE诱导失败以及oxyR和rpoS诱导失败导致细胞内H₂O₂清除能力水平较低所致。

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