July 2019
Volume 60, Issue 9
Open Access
ARVO Annual Meeting Abstract  |   July 2019
Resveratrol protects against hydroquinone-induced damage in RPE cells
Author Affiliations & Notes
  • Samantha Erin Neal
    Ophthalmology, Duke University Eye Center, Durham, North Carolina, United States
  • Kristen Buehne
    Ophthalmology, Duke University Eye Center, Durham, North Carolina, United States
  • Peter Silinski
    Chemistry, Duke University, Durham, North Carolina, United States
  • Ping Yang
    Ophthalmology, Duke University Eye Center, Durham, North Carolina, United States
  • Glenn Jaffe
    Ophthalmology, Duke University Eye Center, Durham, North Carolina, United States
  • Footnotes
    Commercial Relationships   Samantha Neal, None; Kristen Buehne, None; Peter Silinski, None; Ping Yang, None; Glenn Jaffe, None
  • Footnotes
    Support  NIH 5P30EY005722 (Core Grant); Research to Prevent Blindness
Investigative Ophthalmology & Visual Science July 2019, Vol.60, 1942. doi:
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      Samantha Erin Neal, Kristen Buehne, Peter Silinski, Ping Yang, Glenn Jaffe; Resveratrol protects against hydroquinone-induced damage in RPE cells. Invest. Ophthalmol. Vis. Sci. 2019;60(9):1942.

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

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Abstract

Purpose : Oxidative stress in retinal pigment epithelial (RPE) cells is associated with age-related macular degeneration (AMD). Resveratrol exerts a range of protective biologic effects, but its mechanism is not well understood. We investigated how resveratrol could protect RPE cells from hydroquinone, a major oxidant in cigarette smoke, by assessing cell viability, mitochondrial function, cellular antioxidant response, and resveratrol-oxidant interactions.

Methods : Cultured donor RPE cells were treated with hydroquinone (HQ, 150-200µM) and tert-butyl hydroperoxide (t-BHP, 500-900µM) in the presence or absence of resveratrol (Res, 30µM) for four hours. Cell morphology was assessed by light microscopy, and cell viability was determined with WST-1 reagent. Mitochondrial bioenergetics were measured with the Seahorse XF Cell Mito Stress Test. Expression of antioxidant genes heme oxygenase-1 (HO-1) and glutamate-cysteine ligase catalytic subunit (GCLC) was evaluated by PCR. HPLC and mass spectroscopy analyses were performed to monitor a potential interaction between HQ and Res with t-BHP and Res as a comparison.

Results : RPE cells treated with Res had improved cell morphology and significantly increased cell viability compared to cells treated with HQ alone and t-BHP alone (p < 0.05). Res treatment significantly improved mitochondrial function through increased ATP production (p < 0.001) and basal respiration (p < 0.05) compared to HQ alone. Additionally, Res significantly upregulated HO-1 and GCLC expression compared to treatment with HQ alone (p < 0.001). HQ and Res, but not t-BHP and Res, react in solution to form three novel compounds with distinct molecular weights.

Conclusions : RPE cells treated with Res were protected from oxidant injury, as shown by enhanced cell viability, morphology, mitochondrial function, and antioxidant gene expression. The mechanism by which Res exerts its protective effect appears to be oxidant-specific. This study provides insight into some of the pathways through which Res can rescue RPE cells from oxidative damage, an early feature in the pathogenesis of AMD.

This abstract was presented at the 2019 ARVO Annual Meeting, held in Vancouver, Canada, April 28 - May 2, 2019.

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