DNA polymerase I is crucial for the repair of potentially lethal damage caused by the indirect effects of X irradiation in Escherichia coli.
The radiosensitivity of an Escherichia coli mutant deficient in DNA polymerase I was measured in the presence of OH radical scavengers. The extreme X-ray sensitivity of the mutant could be abolished by OH radical scavengers if a sufficiently high level of radioprotector was present. There was a direct correlation between the OH radical scavenging activity of the chemicals tested (NO2-, n-butanol, glycerol, t-amyl alcohol, and t-butanol) and their protective ability. I interpret the data as showing that the indirect actions of X rays (primarily OH radicals) result in major damage to the bacterial DNA which in large part consists of potentially lethal lesions. This potentially lethal damage is repaired through an enzymatic pathway requiring DNA polymerase I. In the mutant lacking DNA polymerase I, these potentially lethal lesions are expressed as cell lethality.
D020001:1-Butanol; D000440:Butanols / Q000494:pharmacology; D004256:DNA Polymerase I / Q000502:physiology*; D004260:DNA Repair; D004269:DNA, Bacterial / Q000528:radiation effects*; D004305:Dose-Response Relationship, Drug; D004926:Escherichia coli / Q000201:enzymology / Q000235:genetics* / Q000528:radiation effects; D005990:Glycerol / Q000494:pharmacology; D006878:Hydroxides; D017665:Hydroxyl Radical; D009154:Mutation; D000439:Pentanols / Q000494:pharmacology; D020002:tert-Butyl Alcohol
D000440:Butanols; D004269:DNA, Bacterial; D006878:Hydroxides; D000439:Pentanols; D017665:Hydroxyl Radical; C032765:tert-amyl alcohol; D020001:1-Butanol; D004256:DNA Polymerase I; D020002:tert-Butyl Alcohol; D005990:Glycerol