Abstract
To identify dietary phenolic compounds capable of improving vitamin E status, male Sprague-Dawley rats were fed for 4 weeks either a basal diet (control) with 2 g/kg cholesterol and an adequate content of vitamin E or the basal diet fortified with quercetin (Q), (-)-epicatechin (EC), or (+)-catechin (C) at concentrations of 2 g/kg. All three catechol derivatives substantially increased concentrations of alpha-tocopherol (alpha-T) in blood plasma and liver. To study potential mechanisms underlying the observed increase of alpha-T, the capacities of the flavonoids to i) protect alpha-T from oxidation in LDL exposed to peroxyl radicals, ii) reduce alpha-tocopheroxyl radicals (alpha-T (.) ) in SDS micelles, and iii) inhibit the metabolism of tocopherols in HepG2 cells were determined. All flavonoids protected alpha-T from oxidation in human LDL ex vivo and dose-dependently reduced the concentrations of alpha-T (.) . None of the test compounds affected vitamin E metabolism in the hepatocyte cultures. In conclusion, fortification of the diet of Sprague-Dawley rats with Q, EC, or C considerably improved their vitamin E status. The underlying mechanism does not appear to involve vitamin E metabolism but may involve direct quenching of free radicals or reduction of the alpha-T (.) by the flavonoids.
Highlights
Inhibit the metabolism of tocopherols in HepG2 cells were determined
From the intestinal mucosal cells, vitamin E enters the circulation via the lymphatic system incorporated into lipoproteins and is eventually transported to the liver, from which a-T is preferentially secreted into the blood [1]
Previous studies support the notion of a regeneration of a-T from its a-tocopheroxyl radical (a-T) at water-lipid interfaces by dietary phenols [18] in a way reminiscent of that of vitamin C [19]
Summary
All flavonoids protected a-T from oxidation in human LDL ex vivo and dose-dependently reduced the concentrations of a-T. Dietary flavonoids with a catechol structure increase a-tocopherol in rats and protect the vitamin from oxidation in vitro. Flavonoids in general, and Q, EC, and C in particular, have a number of reported functions in vitro and in vivo that are hypothesized to promote health. In vitro, they have the ability, inter alia, to scavenge reactive oxygen and nitrogen species, chelate metal ions, inhibit redox-sensitive transcription factors (e.g., nuclear factor-nB), inhibit the expression of free radical-generating enzymes (e.g., inducible nitric oxide synthase) [16], and, function as strong antioxidants [17]. In agreement with ex vivo findings that C preserves a-T in human plasma [22], we previously reported that it increases a-T levels in rats [23]
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