April 2010
Volume 51, Issue 13
Free
ARVO Annual Meeting Abstract  |   April 2010
Regulation of Oxidative Stress in Light-Induced Retinal Degeneration
Author Affiliations & Notes
  • T. Narimatsu
    Laboratory of Retinal Cell Biology,
    Keio University School of Medicine, Tokyo, Japan
  • T. Kurihara
    Laboratory of Retinal Cell Biology,
    Department of Ophthalmology,
    Keio University School of Medicine, Tokyo, Japan
  • S. Kubota
    Laboratory of Retinal Cell Biology,
    Department of Ophthalmology,
    Keio University School of Medicine, Tokyo, Japan
  • S. Ishida
    Laboratory of Retinal Cell Biology,
    Keio University School of Medicine, Tokyo, Japan
    Department of Ophthalmology, Hokkaido University Graduate School of Medicine, Hokkaido, Japan
  • Y. Ozawa
    Laboratory of Retinal Cell Biology,
    Department of Ophthalmology,
    Keio University School of Medicine, Tokyo, Japan
  • K. Tsubota
    Laboratory of Retinal Cell Biology,
    Department of Ophthalmology,
    Keio University School of Medicine, Tokyo, Japan
  • Footnotes
    Commercial Relationships  T. Narimatsu, None; T. Kurihara, None; S. Kubota, None; S. Ishida, None; Y. Ozawa, None; K. Tsubota, None.
  • Footnotes
    Support  None.
Investigative Ophthalmology & Visual Science April 2010, Vol.51, 1434. doi:https://doi.org/
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      T. Narimatsu, T. Kurihara, S. Kubota, S. Ishida, Y. Ozawa, K. Tsubota; Regulation of Oxidative Stress in Light-Induced Retinal Degeneration. Invest. Ophthalmol. Vis. Sci. 2010;51(13):1434. doi: https://doi.org/.

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

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Abstract

Purpose: : Excessive visible light induces apoptosis of retinal photoreceptor cells. Previous reports show that the cell death is caused by oxidative stress generated through excessive activation of visual cycle. However, our daily light stimuli do not induce photoreceptor cell death. There should be a physiological self-defending system. Our final goal is to find a neuroprotective system. In this study, we decided the threshold stimuli of light exposure which could be overcome by the internal protective system.

Methods: : ICR male mice were dark adapted for 1 night, and then, exposed to 5, 2000, 2500 and 13,000 lux fluorescent light for 1 hour, respectively. The photoreceptor cell damage was evaluated by analyzing the outer nuclear layer (ONL) thickness and the number of TUNEL positive cells in the ONL. Then, retinal function was measured by electroretinogram (ERG). Oxidative stress in the retina was measured using dihydroethidium.

Results: : Decrease in ONL thickness, increase in TUNEL positive cells, and decrease in a-wave amplitude of ERG were observed in the mice after 2500-or 13,000-lux light exposure. Intensity of dihydroethidium staining was upregulated under these conditions. In the 2000 lux-light exposed mice, TUNEL positive cells were slightly observed, but the other 2 parameters did not change.

Conclusions: : The threshold condition which avoided light-induced photoreceptor cell loss and visual function impairment was 1 hour-exposure of 2000 lux-light. Thus, further study to find the neuroprotective system which regulates oxidative stress level should be performed under this condition.

Keywords: photoreceptors • oxidation/oxidative or free radical damage 
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