Investigation of an interactive effect of flavonoids on the antioxidant activity of alpha tocopherol.

摘要

The hypothesis tested was: dietary flavonoids interact with alpha-tocopherol (alpha-TOH) to improve its antioxidant capacity in a living system. This project began with a study of the flavonoid quercetin and alpha-TOH in an in vitro lipid environment, followed by a preliminary in vivo rat study feeding quercetin and alpha-TOH to determine the efficacy of this research and to develop and refine research methods. This was followed by the major study in which growing rats consumed tocopherol deficient or sufficient diets supplemented with quercetin or two additional flavonoids, catechin and epicatechin, a food source of flavonoids, cocoa, or a non-digestible polyphenolic compound, lignin. In both in vivo studies, plasma and various tissues were assayed to determine changes in concentration of alpha-TOH, vitamin A, and an oxidation product occurring when feeding these flavonoids in the presence and absence of tocopherol.;The in vitro system utilized the Oxidative Stability Instrument to determine if the combination of the flavonoid, quercetin, and alpha tocopherol provide an additive or synergistic effect in protecting a highly polyunsaturated oil from oxidation during exposure to controlled heating and aeration. From 0.2 to 20 mM concentrations of alpha tocopherol, the addition of 5, 10, and 20 mM quercetin provided enhanced antioxidant protection, as measured by the OSI, Oxidative Stability Index. Quercetin was a more effective antioxidant in this system than alpha-tocopherol, which was in agreement with earlier in vitro research in our lab. However, the combination of tocopherol and quercetin produced less than an additive effect of each antioxidant alone.;The major study involved feeding seventy-two male SD rats AIN93-G diets sufficient or deficient in tocopherol alone or supplemented with one of five treatment compounds: 5 g. quercetin, 5 g. catechin, 5 g. epicatechin, 10 g. cocoa powder, or 10 g. lignin per kg of diet. In tocopherol sufficient groups, all test compounds significantly increased liver tocopherol as compared to the control. In plasma, tocopherol was significantly increased only in animals supplemented with quercetin and catechin. In adipose tissue, quercetin, catechin, and epicatechin significantly increased tocopherol levels. In the tocopherol deficient groups, tocopherol levels were significantly increased by all test compounds in adipose tissue. Plasma and heart F2-isoprostanes were significantly increased in plasma and hearts of tocopherol deficient animals compared to tocopherol sufficient controls but none of the treatment compounds significantly decreased F2-isoprostanes beyond the protection displayed by alpha-tocopherol (sufficient vs. deficient). In conclusion: these antioxidant compounds, quercetin, catechin, and epicatechin at the levels fed were sufficient to spare tocopherol in these various tissues, but insufficient to alter lipid peroxidation as measured under these experimental conditions. (Abstract shortened by UMI.)