1. Methylglyoxal and other carbohydrate metabolites induce lanthanum-sensitive Ca2+ transients and inhibit growth in E. coli
- Author
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Stephanie Beatrix Matthews, Riffat Naseem, Kenneth Taylor Wann, I. Barry Holland, Anthony K. Campbell, Institut de génétique et microbiologie [Orsay] (IGM), and Université Paris-Sud - Paris 11 (UP11)-Centre National de la Recherche Scientifique (CNRS)
- Subjects
Diol ,Biophysics ,[SDV.BC]Life Sciences [q-bio]/Cellular Biology ,Diacetyl ,medicine.disease_cause ,Biochemistry ,03 medical and health sciences ,chemistry.chemical_compound ,Acetals ,Lanthanum ,medicine ,Carbohydrate fermentation ,Escherichia coli ,[SDV.BBM]Life Sciences [q-bio]/Biochemistry, Molecular Biology ,Drug Interactions ,Calcium Signaling ,Molecular Biology ,030304 developmental biology ,Cell Proliferation ,0303 health sciences ,Dose-Response Relationship, Drug ,Acetoin ,030302 biochemistry & molecular biology ,Methylglyoxal ,Carbohydrate ,Pyruvaldehyde ,Cytosol ,chemistry ,Carbohydrate Metabolism - Abstract
The results here are the first demonstration of a family of carbohydrate fermentation products opening Ca2+ channels in bacteria. Methylglyoxal, acetoin (acetyl methyl carbinol), diacetyl (2,3 butane dione), and butane 2,3 diol induced Ca2+ transients in Escherichia coli, monitored by aequorin, apparently by opening Ca2+ channels. Methylglyoxal was most potent (K(1/2) = 1 mM, 50 mM for butane 2,3 diol). Ca2+ transients depended on external Ca2+ (0.1-10 mM), and were blocked by La3+ (5 mM). The metabolites affected growth, methylglyoxal being most potent, blocking growth completely up to 5 h without killing the cells. But there was no affect on the number of viable cells after 24 h. These results were consistent with carbohydrate products activating a La3+-sensitive Ca2+ channel, rises in cytosolic Ca2+ possibly protecting against certain toxins. They have important implications in bacterial-host cell signalling, and where numbers of different bacteria compete for the same substrates, e.g., the gut in lactose and food intolerance.
- Published
- 2007
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