Resumen:
he 8-oxodeoxyguanine (8-oxodG) repair system participates in the preventionand correction of mutations generated by oxidative DNA damage in prokaryotesand eukaryotes. In this study, we report that Pseudomonas aeruginosa strainsdeficient in this repair mechanism by inactivation of the mutT, mutM and mutYgenes generate a high frequency of cells resistant to the antibiotic ciprofloxacin. In the mutT strain, the increase in ciprofloxacin resistance achieved at threefold minimal inhibitory concentration was about 1600-fold over the wild-type (WT) level, similar to the frequency achieved by the mismatch repair-deficient mutS strain. Molecular analysis of WT, mutT and mutY clones resistant to ciprofloxacin indicated that the nfxB gene was mutated in the majority of the cases, while mutSderived resistant clones were mainly mutated in gyrA and parC genes. Cell viability analysis after treatment with paraquat or hydrogen peroxide indicated that 8-oxodG repair-deficient strains were considerably