Abstract
Prior UV irradiation strongly increased the sensitivity to H2O2 of wild-type E. coli K-12 cells. This synergistic lethal interaction was also observed to a reduced extent in a polA mutant but was absent in uvrA, uvrArecA and xthA mutants. In a recA mutant an antagonist effect was observed. Prior H2O2 treatment did not sensitize the wild-type cells to UV irradiation. Alkaline and neutral sucrose gradient analysis, as well as DNA degradation studies, demonstrated that the synergism is due to the production of DNA double-strand breaks and a block of their repair. The possible mechanism of induction of such lesions is discussed.
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