May 2005
Volume 46, Issue 13
ARVO Annual Meeting Abstract  |   May 2005
Quercetin Protects Retinal Pigment Epithelium Against Oxidative Stress
Author Affiliations & Notes
  • D. Kook
    Ophthalmology, Ludwig–Maximilians–University, Munich, Germany
  • S.G. Priglinger
    Ophthalmology, Ludwig–Maximilians–University, Munich, Germany
  • A. Kampik
    Ophthalmology, Ludwig–Maximilians–University, Munich, Germany
  • U. Welge–Luessen
    Ophthalmology, Ludwig–Maximilians–University, Munich, Germany
  • Footnotes
    Commercial Relationships  D. Kook, None; S.G. Priglinger, None; A. Kampik, None; U. Welge–Luessen, None.
  • Footnotes
    Support  Volker und Vera Doppelfeldstiftung
Investigative Ophthalmology & Visual Science May 2005, Vol.46, 1608. doi:
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      D. Kook, S.G. Priglinger, A. Kampik, U. Welge–Luessen; Quercetin Protects Retinal Pigment Epithelium Against Oxidative Stress . Invest. Ophthalmol. Vis. Sci. 2005;46(13):1608.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract: : Purpose:Oxidative stress seems to be a key factor in the pathogenesis of age related macular degeneration (AMD). Early AMD is characterised by specific changes in the retinal pigment epithelium like cell loss and cellular senescence. In other non ocular cell systems these findings are inducible by oxidative stress. In the present study the protective role of the antioxidant quercetin, which is a major dietary flavonoid, on hydrogen peroxide treatment of RPE cells was investigated in vitro. Methods:Cultured human RPE cells were incubated with different concentrations (1–500 µM) of quercetin for 24 hours. Cells were then treated with 300 µM hydrogen peroxide for 2 hours. Mitochondrial function was measured by using an MTT–assay and cell vitality measured by using a live–dead–staining–assay. Apoptosis was assessed by performing a caspase–3–assay. Senescence of RPE–cells was investigated by beta–galactosidase staining. Results: Hydrogen peroxide caused a significant decrease in mitochondrial function (52,0 %) and in cell vitality (70,6 %), whereas preincubation with 50 µM quercetin diminished this decrease significantly (to 15,2 % and 1,8 %, respectively). Hydrogen peroxide induced activation of caspase–3 was markedly reduced by 10 µM quercetin (52,7 %). After hydrogen peroxide exposure the number of beta–galactosidase positive staining RPE cells was > 90 % whereas in the untreated control only single cells expressed this enzyme (< 5 %). 50 µM quercetin pretreatment prevented the hydrogen peroxide induced increase of beta–galactosidase positive staining of RPE cells (< 5%). Conclusions:These data demonstrate that quercetin is able to protect human RPE cells from oxidative damage and cellular senescence in vitro in a dose dependent matter. Therefore we believe, that the use of antioxidants like quercetin is a promising tool to prevent early AMD.

Keywords: age-related macular degeneration • retinal pigment epithelium • oxidation/oxidative or free radical damage 

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