Abstract
Co-intake of grapefruit juice with drugs results in a substantial increase in oral drug bioavailability. In contrast, DNA damage in target organ induced by a food-derived carcinogen, 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP), was reduced in rats by grapefruit juice intake. Aflatoxin B1-induced DNA damage was also suppressed in rats treated with grapefruit juice and an ethyl acetate extract of grapefruit juice. A significant decrease in hepatic CYP3A content, but not in CYP1A, CYP2C, glutathione S-transferase and microsomal epoxide hydrolase contents was observed in rats after grapefruit juice intake. No significant differences in the portal blood and liver concentrations of aflatoxin B1, nor in blood concentration of PhIP, were observed between control rats and rats ingesting grapefruit juice. Thus, grapefruit juice intake causes suppression of carcinogen-induced DNA damage at least in part through decreased metabolic activation in rat liver.
