Abstract
Escherichia coli expressing SOS-inducing mutant topoisomerase I was utilized to demonstrate that covalent protein-DNA complex accumulation results in oxidative damage. Hydroxyl radicals were detected following mutant topoisomerase induction. The presence of the Fe(2+) chelator 2,2'-dipyridyl and an iscS mutation affecting Fe-S cluster formation protect against topoisomerase I cleavage complex-mediated cell killing.
Publication types
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Research Support, N.I.H., Extramural
MeSH terms
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2,2'-Dipyridyl / pharmacology
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Anti-Bacterial Agents / pharmacology
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Arabinose / pharmacology
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DNA / metabolism
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DNA Topoisomerases, Type I / genetics
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DNA Topoisomerases, Type I / metabolism
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DNA Topoisomerases, Type I / physiology*
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Escherichia coli / drug effects
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Escherichia coli / genetics
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Escherichia coli / metabolism*
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Hydroxyl Radical / metabolism*
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Iron Chelating Agents / pharmacology
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Mutation
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Norfloxacin / pharmacology
Substances
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Anti-Bacterial Agents
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Iron Chelating Agents
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Hydroxyl Radical
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2,2'-Dipyridyl
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DNA
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Arabinose
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DNA Topoisomerases, Type I
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Norfloxacin