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Three classes of bactericidal antibiotics induce oxidative damages in addition to their interactions with specific intracellular targets. By utilizing knockout strains of Escherichia coli that lack antioxidant enzymes, we investigated whether deficiencies in the oxidant scavenging pathways would render the mutants more susceptible to ampicillin, norfloxacin and tobramycin. Although the antibiotics mediated detectable increase in oxidative stress, abolishing each of the antioxidant enzymes, manganese superoxide dismutase, hydroperoxidase I or alkyl hydroperoxide reductase did not increase the antibiotic susceptibilities of E. coli. We concluded each of the three enzymes by itself was not essential in the defense against antibiotic-mediated killing.
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Lee et al. (2026) studied this question.
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