Trimethoprim was more potent than zidovudine as an inducer of the SOS response in Escherichia coli. The level of induction by each compound initially increased with rising drug concentration and then fell; this effect was less marked with zidovudine than with trimethoprim. The SOS response did not appear to be involved in the inhibition of bacterial multiplication as the MICs of trimethoprim or zidovudine for recA430 and lexA3 mutants, which are unable to induce the SOS response, were identical to the MICs for the parent strains. However, the bactericidal activity of each compound against strains deficient in the SOS response was reduced. This suggests that induction of the DNA repair system contributes to the bactericidal activity of the drugs.
HuismanO.,
D’AriR,
GottesmanS. Cell-division control in Escherichia coli: specific induction of the SOS function sfiA protein is sufficient to block septation. Proc Natl Acad Sci USA1984; 81:4490–4494
MizusawaS.,
GottesmanS. Protein degradation in Escherichia coli: the Ion gene controls the stability of sulA protein. Proc Natl Acad Sci USA1983; 80:358–362
ElwellL. P.,
FeroneR.,
FreemanG. A. Antibacterial activity and mechanism of action of 3′-azido-3′-deoxythymidine (BW A509U). Antimicrob Agents Chemother1987; 31:274–280
McDanielL. S.,
RogersL. H.,
HillW. E. Survival of recombination-deficient mutants of Escherichia coli during incubation with nalidixic acid. J Bacteriol1978; 134:1195–1198
DeitzW. H.,
CookT. M.,
GossW. A. Mechanism of action of nalidixic acid on Escherichia coli. Ill Conditions required for lethality. J Bacteriol1966; 91:768–773