Ferguson G P, McLaggan D, Booth I R
Department of Molecular and Cell Biology, University of Aberdeen, Marischal College, UK.
Mol Microbiol. 1995 Sep;17(6):1025-33. doi: 10.1111/j.1365-2958.1995.mmi_17061025.x.
Escherichia coli possesses two glutathione-gated potassium channels, KefB and KefC, that are activated by glutathione-S-conjugates formed with methylglyoxal. We demonstrate that activation of the channels leads to cytoplasmic acidification and that this protects cells during electrophilic attack. Further, we demonstrate that mutants lacking the channels can be protected against the lethal effects of methylglyoxal by acidification of the cytoplasm with a weak acid. The degree of protection is determined by the absolute value of the pHi and the time at which acidification takes place. Alterations in the pHi do not accelerate the rate of detoxification of methylglyoxal. The mechanism by which methylglyoxal causes cell death and the implications for pHi-mediated resistance to methylglyoxal are discussed.
大肠杆菌拥有两种谷胱甘肽门控钾通道,即KefB和KefC,它们由与甲基乙二醛形成的谷胱甘肽-S-缀合物激活。我们证明,通道的激活会导致细胞质酸化,并且这在亲电攻击期间保护细胞。此外,我们证明,缺乏这些通道的突变体可以通过用弱酸使细胞质酸化来抵御甲基乙二醛的致死作用。保护程度由细胞内pH值(pHi)的绝对值以及酸化发生的时间决定。细胞内pH值的改变不会加速甲基乙二醛的解毒速率。本文讨论了甲基乙二醛导致细胞死亡的机制以及细胞内pH值介导的对甲基乙二醛抗性的意义。