Hartman P S, Eisenstark A
J Bacteriol. 1978 Feb;133(2):769-74. doi: 10.1128/jb.133.2.769-774.1978.
Wild-type cells and six DNA repair-deficient mutants (lexA, recA, recB, recA, recB, polA1, and uvrA) of Escherichia coli K-12 were treated with near-ultraviolet radiation plus hydrogen peroxide (H2O2). At low H2O2 concentrations (6 X 10(-6) to 6 X 10(-4) M), synergistic killing occurred in all strains except those containing a mutation in recA. This RecA-repairable damage was absent from stationary-phase cells but increased in logarithmic cells as a function of growth rate. At higher H2O2 concentrations (above 6 X 10(-4) M) plus near-ultraviolet radiation, all strains, including those with a mutation in recA, were synergistically killed; thus, at high H2O2 concentrations, the damage was not RecA repairable.
用近紫外辐射加过氧化氢(H₂O₂)处理大肠杆菌K - 12的野生型细胞和六个DNA修复缺陷突变体(lexA、recA、recB、recA、recB、polA1和uvrA)。在低H₂O₂浓度(6×10⁻⁶至6×10⁻⁴M)下,除含有recA突变的菌株外,所有菌株均出现协同杀伤作用。这种可被RecA修复的损伤在稳定期细胞中不存在,但在对数期细胞中随生长速率增加。在较高H₂O₂浓度(高于6×10⁻⁴M)加近紫外辐射时,所有菌株,包括那些含有recA突变的菌株,均被协同杀伤;因此,在高H₂O₂浓度下,损伤不能被RecA修复。