UV Lesions In DNA Research Articles

Differential effects of acriflavine and caffeine on various ultraviolet-irradiated Escherichia coli strains and T1 phage.

Abstract Caffeine and acriflavine are known to inhibit repair of UV lesions in DNA of host-cell-reactivating [HCR(+)] Escherichia coli strains. Large differences were observed between various strains: B, B/r(λ) and K12(λ), carrying extra UV sensitivity relative to B/r and K12S, respectively, show much greater repair inhibition than the latter strains. This seems to be related to the (normally) rather incomplete repair in B, B/r(λ) and K12(λ), which was inferred from results on liquid-holding recovery 6 . Both incompleteness of repair and its great susceptibility to inhibition by caffeine or acriflavine could be explained by the assumption that UV lesions related to the extra sensitivity require the repair early . This assumption seems plausible at least for the extra sensitivity resulting from lysogenicity. Decreased UV survival in the presence of acriflavine or caffeine was also found in HCR(−) strains. B s−1 and B syn − , differing considerably in their UV sensitivities, show equal survival (at levels between 1 and 10 −4 ) if incubated with 7.5 ωg/ml acriflavine. The possible interpretation that all HCR(−) strains tested exhibit residual repair activity in the absence of acriflavine or caffeine, is supported by the finding that HCR(−) strains also show a slight residual HCR activity, inhibitable by acriflavine or caffeine, toward UV-irradiated phage Tr. However, part of the decreased cell survival might be due to synergistic effects between UV and acriflavine. At the highest applicable concentration, acriflavine is a stronger repair inhibitor than caffeine. However, neither substance decreases UV survival of HCR(+) cells or phage infecting HCR(+) cells to the level to which survival of HCR(−) cells or phage infecting HCR(−) cells is decreased by acriflavine or caffeine.