Inhibitory effect of phenolic compounds on aflatoxin B1 metabolism and induced mutagenesis |
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| Institution: | 1. R&D Center, NH Foods Ltd., 3-3 Midorigahara, Tsukuba, Ibaraki 300-2646, Japan;2. Faculty of Agriculture and Graduate School of Agriculture, Kagawa University, 2393 Ikenobe, Miki, Kagawa 761-0795, Japan;1. School of Life Science, Undergraduate and Graduate Programs of Nutrition Science, National Taiwan Normal University, Taipei, Taiwan;2. Group of Food Proteins, Instituto de Investigación en Ciencias de la Alimentación (CIAL, CSIC-UAM, CEI UAM+CSIC), Madrid, Spain;3. Department of Nutritional Science and Toxicology, University of California Berkeley, Berkeley, California, United States |
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| Abstract: | The interaction between phenolic compounds and the food-borne carcinogenic mycotoxin, aflatoxin B1 (AFB1), was examined. 6 phenolic compounds (gallic acid, chlorogenic acid, caffeic acid, dopamine, p-hydroxybenzoic acid and salicyclic acid) inhibited AFB1-induced mutagenesis in Salmonella typhimurium strain TA98 in a suspension assay in the presence of rat-liver microsomes (S9). The inhibitory effect was observed when the phenolic compound and the mutagen (AFB1 plus S9) were administered concurrently, but not when exposure to the mutagen was followed by the phenolic compound. The concentrations of the phenolic compounds used were not mutagenic to S. typhimurium strain TA98 and had no effect on the survival of the bacteria. The inhibition of AFB1 metabolism was studied using high-pressure liquid chromatography. Increasing the concentration of all 6 phenolic compounds resulted in a dose-dependent reduction of both major AFB1 metabolite peaks. The results are consistent with the hypothesis that (1) the phenolic compounds do not react covalently with AFB1, and (2) the inhibitory effect of phenolic compounds on AFB1-induced mutagenesis may be due to the inhibition of the activation enzymes. |
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