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<span style = 'font-size: large'> '''Ferguson, GP, McLaggan, D and Booth, IR'''  (1995) Potassium channel activation by glutathione-S-conjugates in Escherichia coli: protection against methylglyoxal is mediated by cytoplasmic acidification.''Mol. Microbiol.'' '''17''':1025-33</span>
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|{{TableHeadingColor}} |'''Abstract''' || <protect>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.</protect>
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'''Ferguson, GP, McLaggan, D and Booth, IR''' (1995) Potassium channel activation by glutathione-S-conjugates in Escherichia coli: protection against methylglyoxal is mediated by cytoplasmic acidification. ''Mol. Microbiol.'' '''17''':1025-33
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!align=left  |Abstract
*  [http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=8594323 PubMed]
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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.
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[http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=8594323 PubMed]


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Acetates/pharmacology; Acetic Acid; Antiporters/drug effects; Antiporters/genetics; Antiporters/metabolism; Bacterial Proteins/drug effects; Bacterial Proteins/genetics; Bacterial Proteins/metabolism; Chemistry, Physical; Cytoplasm/chemistry; Escherichia coli/drug effects; Escherichia coli/metabolism; Escherichia coli Proteins; Glutathione/physiology; Hydrogen-Ion Concentration; Intracellular Fluid/chemistry; Oxidative Stress; Physicochemical Phenomena; Potassium/metabolism; Potassium Channels/drug effects; Potassium Channels/genetics; Potassium Channels/metabolism; Potassium-Hydrogen Antiporters; Protons; Pyruvaldehyde/pharmacology
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Latest revision as of 04:55, 15 September 2013

Citation

Ferguson, GP, McLaggan, D and Booth, IR (1995) Potassium channel activation by glutathione-S-conjugates in Escherichia coli: protection against methylglyoxal is mediated by cytoplasmic acidification. Mol. Microbiol. 17:1025-33

Abstract

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.

Links

PubMed

Keywords

Acetates/pharmacology; Acetic Acid; Antiporters/drug effects; Antiporters/genetics; Antiporters/metabolism; Bacterial Proteins/drug effects; Bacterial Proteins/genetics; Bacterial Proteins/metabolism; Chemistry, Physical; Cytoplasm/chemistry; Escherichia coli/drug effects; Escherichia coli/metabolism; Escherichia coli Proteins; Glutathione/physiology; Hydrogen-Ion Concentration; Intracellular Fluid/chemistry; Oxidative Stress; Physicochemical Phenomena; Potassium/metabolism; Potassium Channels/drug effects; Potassium Channels/genetics; Potassium Channels/metabolism; Potassium-Hydrogen Antiporters; Protons; Pyruvaldehyde/pharmacology

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