Shiga toxin-producing Escherichia coli (STEC) may cause bloody diarrhea and hemorrhagic colitis, with sometimes severe complications. Because genes coding for Shiga toxins are located on lambdoid prophages, effective toxin production occurs only after prophage induction. However, although agents that effectively induce prophage lambda (a paradigm of the family of lambdoid phages) under laboratory conditions, such as UV irradiation or DNA replication inhibitors, are well known, it is unlikely that such factors are present in human intestine infected with STEC. In this report, we demonstrate that induction of a Shiga toxin-converting prophage in its host (E. coli O157:H7) occurs not only in the presence of DNA-interfering antibiotics (mitomycin C and norfloxacin) but also under conditions of oxidative stress [following treatment with hydrogen peroxide (H(2)O(2))]. Under these conditions, we observed not only effective prophage induction but also expression of the reporter gene (replacing the original stx2 gene). In the light of previously published reports, indicating that oxidative stress conditions might occur during colonization of human intestine by enteric bacteria, and that neutrophil-produced H(2)O(2) can increase production of the Shiga toxin in a clinical isolate of STEC, these results suggest that oxidative stress may be one of the agents responsible for stimulating the pathogenicity determinants of STEC, leading to induction of Shiga toxin-converting prophages in these bacteria.