Antimutagenesis of β-Carotene to Mutations Induced by Quinolone on Salmonella typhimurium

Background one-induced mutagenesis in the Salmonella typhimurium hisG48 strains suggests that these antibiotics are oxygen free radical generators. The use of β-carotene as antioxidant was evaluated as an alternative to reduce oxidative cell damage in patients who need therapy with nalidixic acid, norfloxacin, or pipemidic acid. The studied β-carotene (30%), used by pharmaceutical laboratories as dietary complements, was not toxic or mutagenic for the S. typhimurium TA102 strain at a dose equivalent to 1,500 I.U. At the studied concentrations, the evaluated antimutagen did not modify the minimum inhibitory concentration of nalidixic acid, norfloxacin, or pipemidic acid against uropathogenic Escherichia coli strains. s tagenic effect of nalidixic acid and norfloxacin against hisG48 strains was inhibited with 1500 I.U. of β-carotene. The antimutagenic effect of β-carotene against mutations induced by pipemidic acid was observed even with 150 I.U. of β-carotene. The antimutagenic effect against mutations induced on S. typhimurium TA102 or TA104 strains was observed only when the aroclor 1254 rat-induced liver S9 mixture was used. s ntimutagenic effect was detected only when the strains were exposed to quinolones and the β-carotene simultaneously with the S9 mixture, suggesting that quinolones induce oxygen free radicals that may be scavenged by β-carotene. sions timutagenic effect of this vitamin A precursor is probably due to the active molecule of vitamin A, a desmutagen with the ability of radical capture. A diet rich in β-carotene or vitamin A could be a good alternative to reduce genotoxic risk to patients being treated with quinolone.