POTASSIUM CHANNEL ACTIVATION BY GLUTATHIONE-S-CONJUGATES IN ESCHERICHIA-COLI - PROTECTION AGAINST METHYLGLYOXAL IS MEDIATED BY CYTOPLASMIC ACIDIFICATION
POTASSIUM CHANNEL ACTIVATION BY GLUTATHIONE-S-CONJUGATES IN ESCHERICHIA-COLI - PROTECTION AGAINST METHYLGLYOXAL IS MEDIATED BY CYTOPLASMIC ACIDIFICATION
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DOI：
10.1111/j.1365-2958.1995.mmi_17061025.x
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发表时间：
1995-09-01
影响因子：
3.6
通讯作者：
BOOTH, IR
中科院分区：
文献类型：
--
作者：
FERGUSON, GP;MCLAGGAN, D;BOOTH, IR
大肠杆菌具有两个谷胱甘肽门控钾通道，KefB和KefC，其被与甲基乙二醛形成的谷胱甘肽-S-缀合物激活。我们证明，激活的通道导致细胞质酸化，这保护细胞在亲电攻击。此外，我们证明，突变体缺乏通道可以保护免受致命的影响，丙酮醛的细胞质酸化与弱酸。保护程度由pH（i）的绝对值和酸化发生的时间决定。改变pH值（i）不会加快丙酮醛的解毒速度。甲基乙二醛引起细胞死亡的机制和pH（i）介导的甲基乙二醛耐药性的影响进行了讨论。
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 pH(i) and the time at which acidification takes place. Alterations in the pH(i) do not accelerate the rate of detoxification of methylglyoxal. The mechanism by which methylglyoxal causes cell death and the implications for pH(i)-mediated resistance to methylglyoxal are discussed.