San R H, Chan R I
Mutat Res. 1987 Apr;177(2):229-39. doi: 10.1016/0027-5107(87)90005-4.
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.
研究了酚类化合物与食源性致癌霉菌毒素黄曲霉毒素B1（AFB1）之间的相互作用。在大鼠肝脏微粒体（S9）存在的情况下，通过悬浮试验检测了6种酚类化合物（没食子酸、绿原酸、咖啡酸、多巴胺、对羟基苯甲酸和水杨酸）对AFB1诱导鼠伤寒沙门氏菌TA98菌株发生诱变的抑制作用。当酚类化合物与诱变剂（AFB1加S9）同时给药时观察到抑制作用，但在接触诱变剂后再给予酚类化合物时则未观察到抑制作用。所用酚类化合物的浓度对鼠伤寒沙门氏菌TA98菌株无诱变作用，且对细菌的存活无影响。使用高压液相色谱法研究了AFB1代谢的抑制情况。增加所有6种酚类化合物的浓度会导致主要AFB1代谢物峰呈剂量依赖性降低。这些结果与酚类化合物不与AFB1发生共价反应的假设一致，酚类化合物对AFB1诱导诱变的抑制作用可能是由于对活化酶的抑制。
