Antimutagenesis of beta-carotene to mutations induced by quinolone on Salmonella typhimurium

Background. Quinolone-induced mutagenesis in the Salmonella typhimurium his G48 strains suggests that these antibiotics are oxygen free radical generat ors. The use of beta-carotene as antioxidant was evaluated as an alternativ e to reduce oxidative cell damage in patients who need therapy with nalidix ic acid, norfloxacin, or pipemidic acid. The studied beta-carotene (30%), u sed by pharmaceutical laboratories as dietary complements, was not toxic or mutagenic for the S, typhimurium TA102 strain at a dose equivalent to 1,50 0 I.U. At the studied concentrations, the evaluated antimutagen did not mod ify the minimum inhibitory concentration of nalidixic acid, norfloxacin, or pipemidic acid against uropathogenic Escherichia coli strains. Methods. The mutagenic effect of nalidixic acid and norfloxacin against his G48 strains was inhibited with 1500 I.U. of beta-carotene. The antimutageni c effect of beta-carotene against mutations induced by pipemidic acid was o bserved even with 150 I.U. of beta-carotene. The antimutagenic effect again st mutations induced on S. typhimurium TA102 or TA104 strains was observed only when the aroclor 1254 rat-induced liver S9 mixture was used. Results. This antimutagenic effect was detected only when the strains were exposed to quinolones and the beta-carotene simultaneously with the S9 mixt ure, suggesting that quinolones induce oxygen free radicals that may be sca venged by beta-carotene. Conclusions. The antimutagenic effect of this vitamin A precursor is probab ly clue to the active molecule of vitamin A, a desmutagen with the ability of radical capture. A diet rich in beta-carotene or vitamin A could be a go od alternative to reduce genotoxic risk to patients being treated with quin olone. (C) 2000 IMSS. Published by Elsevier Science Inc.