Quercetin-iron chelates are transported via glucose transporters

Evangelia Vlachodimitropoulou, Paul A. Sharp, Richard J. Naftalin

Research output: Contribution to journalArticlepeer-review

68 Citations (Scopus)

Abstract

Flavonoids are well-known antioxidants and free radical scavengers. Their metal-binding activity suggests that they could be effective protective agents in pathological conditions caused by both extracellular and intracellular oxidative stress linked to metal overload. Quercetin is both a permeant ligand via glucose transport proteins (GLUTS) and a high-affinity inhibitor of GLUT-mediated glucose transport. Chelatable "free iron" at micromolar concentrations in body fluids is a catalyst of hydroxyl radical (OH center dot) production from hydrogen peroxide. A number of flavonoids, e.g., quercetin, luteolin, chrysin, and 3,6-dihydroxyflavone, have been demonstrated to chelate intracellular iron and suppress OH center dot radical production in Madin Darby canine kidney cells. The most effective chelation comes from the flavonone B ring catechol found in both quercetin and luteolin. We show here that quercetin concentrations of 1 mu M) or GLUT inhibitors, e.g., phloretin or cytochalasin B, and iron efflux is enhanced by impermeant extracellular iron chelators, either desferrioxamine or rutin. This iron shuttling property of quercetin might be usefully harnessed in chelotherapy of iron-overload conditions. (C) 2011 Elsevier Inc. All rights reserved.
Original languageEnglish
Pages (from-to)934 - 944
Number of pages11
JournalFree Radical Biology and Medicine
Volume50
Issue number8
DOIs
Publication statusPublished - 15 Apr 2011

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