The induction of several SOS genes of Escherichia coli by fluoroquinolones has been studied. Three different SOS gene fusions (recA::lacZ, umuC::lacZ and sulA::lacZ) have been introduced into the E.coli MC1061 strain to study the induction of these SOS genes in the same genetic background. Data on the basal level of expression of these fusions, as well as their induction by mitomycin C and N-methyl-N'-nitro-N-nitrosoguanidine are presented. Using these strains, we have found that, like nalidixic acid, ofloxacin, enoxacin and ciprofloxacin are strong inducers of the SOS genes tested, umuC gene expression being the highest. Furthermore, fluoroquinolones produced a significant increase in the reversion of the base substitution hisG428 mutation in the TA102 Salmonella tester strain, while no effect was found in strains TA98, TA100, TA1537 and TA1535. These data indicate that the error-prone repair pathway can participate in mutagenesis induced by fluoroquinolones and also that the damage produced by these chemicals may be similar to that produced by nalidixic acid.

No abstract

No abstract

A fusion between the promoter of the nrdA gene of Escherichia coli and the lacZ gene has been constructed, and the induction of nrdA gene expression by 20 organic and 20 inorganic chemicals has been studied. The inducing compounds of the SOS genes, such as bleomycin, captan, ciprofloxacin, enoxacin, hydroxyurea, N-methyl-N'-nitro-N-nitrosoguanidine, mitomycin C, nalidixic acid, ofloxacin and hexavalent chromium compounds also trigger the expression of the nrdA gene. Other chemicals such as aluminium, manganese and zinc salts, reported as negative in the SOS Chromotest, are also inducers of the nrdA gene. These results suggest that ribonucleoside diphosphate reductase transcription is increased by chemicals able to either block DNA synthesis or to alter the enzymes participating in the DNA replication. Induction of nrdA gene is an effect to be further considered in the study of alterations produced by physical or chemical treatments which act upon DNA metabolism.

No abstract