Pretreatment with 2.5 mM H2O2 protects bacterial cells against UV killing, a phenomenon that is independent of the SOS response. This protection possibly involves the induction of some other DNA repair mechanism, since lexA (Ind(-)) mutants pretreated with this concentration of H2O2 enhance the repair of UV-damaged phages. Moreover, the induction of this DNA repair mechanism is independent of the oxyR regulon. However, the repair of UV-damaged phages is not enhanced in recA and uvrA mutants, suggesting a DNA repair mechanism independent of LexA cleavage or OxyR activation, but dependent on RecA and UvrA proteins.