Abstract
Erythrose inhibited the growth of a sodA sodB strain of Escherichia coli under aerobiosis; but did not inhibit anaerobic growth of the sodA sodB strain, or the aerobic growth of the superoxide dismutase (SOD)-competent parental strain. A SOD mimic protected the sodA sodB strain against the toxicity of erythrose as did the carbonyl-blocking reagents hydrazine and aminoguanidine. Three carbon sugars, such as glyceraldehyde and dihydroxy acetone, and the two carbon sugar glycolaldehyde, were similarly toxic in an O-2-dependent manner. An unidentified dialyzable component in E. coli extract augmented the oxidation of short chain sugars, and this was partially inhibitable by SOD. The toxicity of the short chain sugars appears to be because of an O-2-dependent oxidation to alpha, beta-dicarbonyl compounds. In keeping with this view was the O-2-independent toxicity of methylglyoxal.
Highlights
During an attempt to use erythrose as a carbon source for the growth of a sodA sodB strain of Escherichia coli, we noted an oxygen-dependent toxicity and set out to explore its mechanism
Erythrose Toxicity Is Dependent on O2.—Erythrose dose-dependently inhibited the growth of a sodA sodB strain of E. coli, as shown in Fig. 1 by lines 3, 2, and 1
The SOD1-competent parental strain was much less affected. This suggested that an oxidation of erythrose initiated by, and/or producing, O2. was a factor in this toxicity
Summary
During an attempt to use erythrose as a carbon source for the growth of a sodA sodB strain of Escherichia coli, we noted an oxygen-dependent toxicity and set out to explore its mechanism. In the toxicities of erythrose and shorter chain sugars. The data reported indicate a role for O2. These results are relevant to the much slower process of nonenzymic glycation seen with long chain sugars, such as glucose, which exist primarily as internal hemiacetals and are less reactive [11,12,13,14,15]
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