Inhibition of microsomal activation of aflatoxin B1 by 3-dehydroretinol and 3-dehydroretinyl palmitate.

Two vitamin A2 compounds (3-dehydroretinol and 3-dehydroretinyl palmitate) which are predominantly present in fresh water fish have been found to be very effective in inhibiting the microsome catalysed formation of DNA adduct by the carcinogen aflatoxin B1. The inhibition appears to be due to modulation of microsomal enzymes which activate the carcinogen. Such inhibition may suggest a potential chemopreventive role of these compounds against carcinogenesis induced by aflatoxin B1.

Action of curcumin on the cytochrome P450-system catalyzing the activation of aflatoxin B1.

Curcumin, in a dose-dependent manner, inhibited the formation of covalent adduct between aflatoxin B1 and DNA, as catalyzed by microsomes or a reconstituted microsomal monooxygenase system. Its effect on the cytochrome P450-system was investigated in the latter system. The inhibition (50%) of aflatoxin B1-DNA adduct formation by curcumin in this system could be reversed by increasing the amount of cytochrome P450 but not by that of NADPH-cytochrome P450 reductase.

In vivo effect of dietary factors on the molecular action of aflatoxin B1: role of non-nutrient phenolic compounds on the catalytic activity of liver fractions.

Young adult rats were kept on a synthetic diet containing various food associated phenolic compounds each at 0.5% level. The ability of liver microsomes to catalyze reactions of aflatoxin B1 leading to its activation and DNA adduct formation was measured after an experimental feeding period of 3 weeks.

Modulatory effects of essential oils from spices on the formation of DNA adduct by aflatoxin B1 in vitro.

Essential oils from common spices such as nutmeg, ginger, cardamom, celery, xanthoxylum, black pepper, cumin, and coriander were tested for their ability to suppress the formation of DNA adducts by aflatoxin B1 in vitro in a microsomal enzyme-mediated reaction. All oils were found to inhibit adduct formation very significantly and in a dose-dependent manner. The adduct formation appeared to be modulated through the action on microsomal enzymes, because an effective inhibition on the formation of activated metabolite was observed with each oil.

In vivo effect of dietary factors on the molecular action of aflatoxin B1: role of riboflavin on the catalytic activity of liver fractions.

Weanling rats were kept on a synthetic riboflavin-free diet for 4 weeks, and subsequently on the same diet but supplemented with riboflavin for 2 weeks. The ability of liver microsomes to catalyze reactions of aflatoxin B1 (AFB1) leading to its activation and DNA adduct formation was measured after each period of experimental feeding. A decrease in both activities was evident during riboflavin deficiency, and this could be restored after normal supply of the vitamin.