The mutagenic activity of ozone was investigated by the isolation of streptomycin-resistant mutants (Smr) in different strains of Escherichia coli. RecA, lexA, polA and parental strains were ozonated and streptomycin-resistant mutants were scored after a short or long phenotypic delay. Our results suggest that ozone is an active mutagen for forward mutation and that this oxidizing agent could be able to induce mutations via two mechanisms: directly and indirectly by the rec-lex error-prone repair system.

No abstract

Ozone was tested for its effect upon induction of lambda prophage in two different strains of Escherichia coli K-12. Based on the induction index and when compared to ultraviolet light, ozone appeared to be a weak, if any at all, inducer of the lytic cycle in E. coli. This is in agreement with other studies which have suggested that this agent is a weak inducer of the SOS functions.

Host cell reactivation capacity for ozonated or irradiated phage was determined for different strains of E. coli either more sensitive or resistant to ozone than the wild type strain. The results suggest that the ozr gene product could be involved in the same repair pathway for ozone-induced lesions on DNA as the polA gene. The possible involvement of a specific endonuclease for these lesions is also considered.