Dietary flavonoids with a catechol structure increase α-tocopherol in rats and protect the vitamin from oxidation in vitro

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), (2)-epicatechin (EC), or (1)-catechin (C) at concentrations of 2 g/kg. All three catechol derivatives substantially increased concentrations of a-tocopherol (a-T) in blood plasma and liver. To study potential mechanisms underlying the observed increase of a-T, the capacities of the flavonoids to i ) protect a-T from oxidation in LDL exposed to peroxyl radicals, ii ) reduce a-tocopheroxyl radicals (a-T˙) in SDS micelles, and iii ) inhibit the metabolism of tocopherols in HepG2 cells were determined. All flavonoids protected a-T from oxidation in human LDL ex vivo and dose-dependently reduced the concentrations of a-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 a-T˙by the

Physiological levels of tea catechins increase cellular lipid antioxidant activity of vitamin C and vitamin E in human intestinal Caco-2 cells

“…Our cell observation is consistent with the prediction and observations made in the cell-free condition. Catechins and phenolic acid were shown to regenerate vitamin E effectively [48][49][50][51][52]. Polyphenols were found to further delay Cu +2 -mediated LDL oxidation when added with vitamin C and vitamin E [42].…”

“…Polyphenols were found to further delay Cu +2 -mediated LDL oxidation when added with vitamin C and vitamin E [42]. Feeding catechins has been shown to increase plasma and liver α-tocopherol concentration in rats [52].…”

LDL Isolated from Plasma-Loaded Red Wine Procyanidins Resist Lipid Oxidation and Tocopherol Depletion

“…This has been subsequently verified for distinct compounds, and evidence for such occurrence in ViVo has been recently forwarded (33). Considering that such an R-TOH recycling mechanism, encompassing the transfer of the radical character from lipid compartments to the water phase, affords a high protection of the lipid systems (LDL, membranes) against oxidation (13), we therefore studied the ability of procyanidins to regenerate R-TOH by reducing R-TO…”

The oral bioavailability of curcuminoids in healthy humans is markedly enhanced by micellar solubilisation but not further improved by simultaneous ingestion of sesamin, ferulic acid, naringenin and xanthohumol

“…Naringenin inhibits phase II enzymes, such as the UDP-glucuronosyltransferase (UGT) 1A1, conjugating curcuminoids with glucuronic acid and membrane transporters exporting glucuronidated metabolites out of intestinal cells (Brand et al, 2006). Sesamin is metabolised by and modulates the activities of phase I and II enzymes, including UGT and catechol-O-methyltransferases (Yasuda et al, 2011), and in our previous animal and human studies significantly inhibited the metabolism and pharmacokinetics of vitamin E (Frank et al, 2006(Frank et al, , 2008Grebenstein, Schumacher, Graeve, & Frank, 2014;Kamal-Eldin et al, 2000;Ross et al, 2004). Xanthohumol is conjugated by UGT and sulphotransferases (Ruefer, Gerhauser, Frank, Becker, & Kulling, 2005) and might thus competitively inhibit the metabolism of curcuminoids by these enzymes.…”