Hartman P S, Eisenstark A
Mutat Res. 1980 Aug;72(1):31-42. doi: 10.1016/0027-5107(80)90217-1.
Near-ultraviolet (NUV) radiation killing of Escherichia coli K-12 can be enhanced by a sub-lethal concentration of hydrogen peroxide. This can be divided into a "RecA-dependent" and "RecA-independent" synergistic killing action. Stationary phase wild-type and 8 closely related repair-deficient mutants were examined for their NUV sensitivities in the presence and absence of H2O2. All exhibited the "RecA-independent" synergism; i.e., H2O2 enhanced NUV lethality when RecA repair was not operating. The "RecA-independent" synergism did not result from destruction of repair enzymes. Very few DNA--protein crosslinks could be detected following NUV plus H2O2 treatment. However, double-strand (DS) DNA breaks were produced, apparently by conversion of closely spaced single-strand (SS) breaks on opposite strands. The correlation between DS-break formation and lethality in wild-type and a polA mutant indicates that the RecA-independent synergistic killing results from the conversion of SS into lethal DS breaks.
近紫外线（NUV）对大肠杆菌K-12的杀伤作用可通过亚致死浓度的过氧化氢增强。这可分为“RecA依赖性”和“RecA非依赖性”协同杀伤作用。研究了稳定期野生型和8个密切相关的修复缺陷型突变体在有和没有过氧化氢存在时的NUV敏感性。所有突变体均表现出“RecA非依赖性”协同作用；即，当RecA修复不起作用时，过氧化氢增强了NUV的致死性。“RecA非依赖性”协同作用并非由修复酶的破坏引起。在NUV加过氧化氢处理后，几乎检测不到DNA-蛋白质交联。然而，双链（DS）DNA断裂产生，显然是由相反链上紧密间隔的单链（SS）断裂转化而来。野生型和polA突变体中DS断裂形成与致死性之间的相关性表明，RecA非依赖性协同杀伤作用是由SS转化为致死性DS断裂所致。
