Abstract
Two modes of killing of Escherichia coli K-12 by hydrogen peroxide can be distinguished. Mode-one killing was maximal with hydrogen peroxide at a concentration of 1 to 2 mM. At higher concentrations the killing rate was approximately half maximal and was independent of H2O2 concentration but first order with respect to exposure time. Mode-one killing required active metabolism during the H2O2 challenge, and it resulted in sfiA-independent filamentation of both cells which survived and those which were killed by the challenge. This mode of killing was enhanced in xth, polA, recA, and recB strains and was accelerated in all strains by an unidentified, anoxia-induced cell function. A strain carrying both xth and recA mutations appeared to undergo spontaneous mode-one killing only under aerobic conditions. Mode-one killing appeared to result from DNA damage which normally occurs at a low, nonlethal level during aerobic growth. Mode-two killing occurred at higher doses of H2O2 and exhibited a multihit dependence on both H2O2 concentration and exposure time. Mode-two killing did not require active metabolism, and killed cells did not filament, although survivors demonstrated a dose-dependent growth lag. Strains with DNA-repair defects were not especially susceptible to mode-two killing.
MeSH Terms
Chloramphenicol/pharmacology
DNA Polymerase I/metabolism
DNA Repair
Dose-Response Relationship, Drug
Escherichia coli/drug effects,genetics
Exodeoxyribonucleases/metabolism
Glucose/pharmacology
Hydrogen Peroxide/pharmacology
Kinetics
Oxygen
Time Factors
Chemicals
Chloramphenicol
Hydrogen Peroxide
DNA Polymerase I
Exodeoxyribonucleases
exodeoxyribonuclease III
Glucose
Oxygen
Authors & Affiliations
2 authors, click to expand affiliations / ORCID
Imlay J A
Linn S
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