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The quercetin paradox.

Agnes W Boots1, Hui Li, Roel P F Schins

  • 1Department of Pharmacology and Toxicology, Faculty of Medicine, University of Maastricht, PO Box 616, 6200 MD Maastricht, The Netherlands. a.boots@farmaco.unimaas.nl

Toxicology and Applied Pharmacology
|June 1, 2007
PubMed
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Quercetin, an antioxidant, paradoxically converts into a toxic form that damages lung cells. This study shows this "quercetin paradox" occurs in living cells, highlighting risks of antioxidant supplements.

Area of Science:

  • Biochemistry
  • Cell Biology
  • Toxicology

Background:

  • Antioxidants like quercetin protect against free radicals.
  • Quercetin's oxidation products can be toxic, reacting with thiols and impairing protein function.
  • The "quercetin paradox" describes this conversion into a potentially harmful substance.

Purpose of the Study:

  • To investigate the quercetin paradox in living rat lung epithelial (RLE) cells.
  • To determine if quercetin's protective effects are offset by metabolite toxicity.
  • To elucidate the role of glutathione (GSH) in mediating this paradox.

Main Methods:

  • Exposure of RLE cells to hydrogen peroxide (H2O2) with and without quercetin.
  • Assessment of DNA damage, GSH levels, lactate dehydrogenase (LDH) leakage, and cytosolic free calcium.

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  • Pre-treatment with buthionine sulfoximine (BSO) to deplete GSH.

    • Main Results:

    • Quercetin protected RLE cells against H2O2-induced DNA damage.
    • This protection was accompanied by reduced GSH levels, increased LDH leakage, and elevated cytosolic calcium.
    • Depleting GSH exacerbated the quercetin paradox, confirming the involvement of thiol-reactive metabolites.

    Conclusions:

    • The quercetin paradox occurs in living lung cells, exchanging DNA damage for thiol-related cellular damage.
    • Quercetin metabolites direct oxidative damage towards thiol arylation.
    • Potential toxicity of antioxidant metabolites necessitates careful consideration in supplementation strategies.