Inhibitory effect of phenolic compounds on aflatoxin B1 metabolism and induced mutagenesis.

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 salicylic 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 the phenolic compounds do not react covalently with AFB1, and the inhibitory effect of phenolic compounds on AFB1-induced mutagenesis may be due to the inhibition of the activation enzymes.

Mechanism of inhibition of N-methyl-N'-nitro-N-nitrosoguanidine-induced mutagenesis by phenolic compounds.

At non-toxic concentrations, 2 naturally occurring phenolic compounds, caffeic acid and chlorogenic acid, suppressed the mutagenic activity of the carcinogen N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) in Salmonella typhimurium strain TA1535. The inhibitory effect was observed only when the phenolic compound and the mutagen were administered concurrently. The interaction between phenolic compounds and MNNG was also studied in a cell-free system using a colorimetric method. The results are consistent with the assumption that phenolic compounds scavenge reactive electrophilic MNNG degradation products, thereby preventing their action on critical cellular targets.

Antimutagenic activity of browning reaction products.

The Salmonella typhimurium assay was used to determine the antimutagenic effect of products of 2 non-enzymatic browning reactions obtained by heating a lysine-fructose mixture at 121 degrees C for 1 h and by carmelizing D-sucrose at 180 degrees C for 1.5 h. The antimutagenic effect was tested by exposing strain TA1535 in suspension to N-methyl-N' -nitro-N-Nitrosoguanidine (MNNG) in the presence of the browning reaction products. In the case of aflatoxin B1, strain TA98 was used and the browning reaction products were added to the precarcinogen and an S9 mixture. The mutagenic activity of both carcinogens was significantly suppressed by the browning reaction products.