Difference between revisions of "PMID:10574955"

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'''Nunoshiba, T, Obata, F, Boss, AC, Oikawa, S, Mori, T, Kawanishi, S and Yamamoto, K'''  (1999) Role of iron and superoxide for generation of hydroxyl radical, oxidative DNA lesions, and mutagenesis in Escherichia coli. ''J. Biol. Chem.'' '''274''':34832-7
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!align=left align='left' bgcolor='#CCCCFF' |Abstract
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We measured the generation of hydroxyl radical (OH(.)) and oxidative DNA lesions in aerobically grown Escherichia coli cells lacking in both superoxide dismutases (SodA SodB) and repressor of iron uptake (Fur) using electroparamagnetic resonance and gas chromatography-mass spectrometry with a selected-ion monitoring method. A specific signal corresponding to OH(.) generation and an increase in oxidative DNA lesions such as 7,8-dihydro-8-oxoguanine and 1,2-dihydro-2-oxoadenine were detected in the strain deficient in sodA sodB fur. We showed that iron metabolism deregulation in fur mutant produced a 2.5-fold iron overload. The sodA sodB fur strain was about 100-fold higher mutability than the wild-type strain. The mutation spectrum in the strain was found to induce GC --> TA and AT --> CG transversions predominantly. The hypermutability of the strain was suppressed by the tonB mutation which reduces iron transport. Thus, excess iron and excess superoxide were responsible for OH(.) generation, oxidative DNA lesion formation, and hypermutability in E. coli.
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[http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=10574955 PubMed]
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!align=left align='left' bgcolor='#CCCCFF' |Keywords
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Bacterial Proteins/genetics; Colicins/metabolism; DNA Damage; Drug Resistance, Microbial/genetics; Escherichia coli/genetics; Escherichia coli/metabolism; Escherichia coli Proteins; Genes, Suppressor; Hydroxyl Radical/metabolism; Iron/metabolism; Manganese/metabolism; Membrane Proteins/genetics; Mutagenesis; Point Mutation; RNA, Transfer/genetics; Repressor Proteins/genetics; Rifampin/metabolism; Spin Trapping; Superoxide Dismutase/genetics; Superoxide Dismutase/metabolism; Superoxides/metabolism
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==Main Points of the Paper ==
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== Materials and Methods Used ==
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==Phenotype Annotations==
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!|Phenotype of!!Taxon Information!!Genotype Information (if known)!!Condition Information!!OMP ID!!OMP Term Name!!ECO ID!!ECO Term Name!!Notes!!Status
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==Notes==
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==References==
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[[Category:Publication]]

Latest revision as of 17:59, 15 January 2015

Citation

Nunoshiba, T, Obata, F, Boss, AC, Oikawa, S, Mori, T, Kawanishi, S and Yamamoto, K (1999) Role of iron and superoxide for generation of hydroxyl radical, oxidative DNA lesions, and mutagenesis in Escherichia coli. J. Biol. Chem. 274:34832-7

Abstract

We measured the generation of hydroxyl radical (OH(.)) and oxidative DNA lesions in aerobically grown Escherichia coli cells lacking in both superoxide dismutases (SodA SodB) and repressor of iron uptake (Fur) using electroparamagnetic resonance and gas chromatography-mass spectrometry with a selected-ion monitoring method. A specific signal corresponding to OH(.) generation and an increase in oxidative DNA lesions such as 7,8-dihydro-8-oxoguanine and 1,2-dihydro-2-oxoadenine were detected in the strain deficient in sodA sodB fur. We showed that iron metabolism deregulation in fur mutant produced a 2.5-fold iron overload. The sodA sodB fur strain was about 100-fold higher mutability than the wild-type strain. The mutation spectrum in the strain was found to induce GC --> TA and AT --> CG transversions predominantly. The hypermutability of the strain was suppressed by the tonB mutation which reduces iron transport. Thus, excess iron and excess superoxide were responsible for OH(.) generation, oxidative DNA lesion formation, and hypermutability in E. coli.

Links

PubMed

Keywords

Bacterial Proteins/genetics; Colicins/metabolism; DNA Damage; Drug Resistance, Microbial/genetics; Escherichia coli/genetics; Escherichia coli/metabolism; Escherichia coli Proteins; Genes, Suppressor; Hydroxyl Radical/metabolism; Iron/metabolism; Manganese/metabolism; Membrane Proteins/genetics; Mutagenesis; Point Mutation; RNA, Transfer/genetics; Repressor Proteins/genetics; Rifampin/metabolism; Spin Trapping; Superoxide Dismutase/genetics; Superoxide Dismutase/metabolism; Superoxides/metabolism

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Main Points of the Paper

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Materials and Methods Used

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Phenotype Annotations

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<protect>

Phenotype of Taxon Information Genotype Information (if known) Condition Information OMP ID OMP Term Name ECO ID ECO Term Name Notes Status
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</protect>

Notes

References

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