Abstract
Quercetin (3,3', 4', 5, 7-pentahydroxyflavone), a fiavonol-type fiavonoid present In vegetables, is of much interest as an anti-atherosclerotic food factor. Of all its biologlcal effects, the antioxidant activity seems to play a role in preventing atherosclerosis. However, bioavailability should be clarified to evaluate rightfully the biological effect of food factors. Quercetin frequently exists as its glycoside forms in plant foods. Glucoside-bound quercetin is mostly absorbed and hydrolyzed in small intestine through glucose-transport system or passive transport after lactase phlorizin hydrolase (LPH)-dependent deglucosidation. Quercetin glycosides other than glucoside forms are likely to be absorbed in large intestine after hydrolysis with enterobacteria. In both cases, resulting quercetin aglycone is converted to conjugated glucuronides and/or sulfates during the process of their absorption. Some metabolites circulating In the blood stream were found to act as free radical scavengers, as well as the inhibitors of lipoxygenase and xanthine oxidase. It Is unlikely that the conjugated metabolites invade into target cells directly because of their lower lipophilicity. However, quercetin aglycone may be again released and incorporated into the cells by the action of p-glucuronidase activity In the process of inflammation. Therefore, dietary quercetin can exert its various biological activities within the cells, as well as in the blood stream. In fact, we recently demonstrated in a rabbit study that dietary quercetin glycoside accumulates as its metabolites in the aorta, and attenuates lipid peroxidation occurring in this target site of anti-atherosclerosis.
