July 2018
Volume 59, Issue 9
Open Access
ARVO Annual Meeting Abstract  |   July 2018
Low LED light exposure as a model of retinal degeneration in Albino rats.
Author Affiliations & Notes
  • Maria Mercedes Benedetto
    Center for Biological Chemistry Research in Cordoba (CIQUIBIC-CONICET), Department of Biological Chemistry "Dr. Ranwell Caputto", School of Chemical Sciences, National University of Cordoba, Cordoba, Cordoba, Argentina
  • Mario Eduardo Guido
    Center for Biological Chemistry Research in Cordoba (CIQUIBIC-CONICET), Department of Biological Chemistry "Dr. Ranwell Caputto", School of Chemical Sciences, National University of Cordoba, Cordoba, Cordoba, Argentina
  • Maria Ana Contin
    Center for Biological Chemistry Research in Cordoba (CIQUIBIC-CONICET), Department of Biological Chemistry "Dr. Ranwell Caputto", School of Chemical Sciences, National University of Cordoba, Cordoba, Cordoba, Argentina
  • Footnotes
    Commercial Relationships   Maria Benedetto, None; Mario Eduardo Guido, None; Maria Contin, None
  • Footnotes
    Support  None
Investigative Ophthalmology & Visual Science July 2018, Vol.59, 1006. doi:https://doi.org/
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      Maria Mercedes Benedetto, Mario Eduardo Guido, Maria Ana Contin; Low LED light exposure as a model of retinal degeneration in Albino rats.. Invest. Ophthalmol. Vis. Sci. 2018;59(9):1006. doi: https://doi.org/.

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

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Abstract

Purpose : Excessive light exposure may accelerate genetic retinal diseases or induce photoreceptor cell (PRC) death, finally leading to retinal degeneration (RD). Light pollution (LP) caused by artificial light may accelerate degenerative diseases or promote RD and circadian desynchrony. In a model of constant LED light exposure at 200 lux we demonstrated classical PRC death with a clear reduction in electroretinogram responses. Rhodopsin (Rho) expression was not altered before PRC death; however, it was more phosphorylated in ser334 than in control animals. Inner retina showed changes in the protein expression and cellular re-localization of melanopsin and neuropsin. In the present study, we investigated the molecular mechanisms involved in ONL cell death, studying the oxidative stress mechanism, rods membranes fatty acids content and whether Rho –phosphorylation is a reversibility mechanism.

Methods : Male Albino Wistar rats (12-15 weeks old) were exposed to constant light (LL); light: dark cycle (0 lx: 200 lx, LD) or constant dark (DD) according experimental design. Cellular redox state was evaluated by reactive oxygen species (ROS) levels quantification by flow cytometer using DCFH/DA and Catalase (CAT) activity assay by spectrophotometry. Fatty acids status was studied by gas chromatography–mass spectrometry (GC-MS) and Rho phosphorylation was evaluated by western blot. Data are expressed as mean ± SD. Statistical comparisons were made using one-way ANOVA; p-value < 0.05 was considered statistically significant. In all cases with significance, a Tukey post hoc test with a p value < 0.05 was considered statistically significant.

Results : After light treatment we found a significant increase in retinal ROS production, however, the enzymatic activity of CAT was not different between groups. GC-MS showed different fatty acid composition between groups. Finally, Rho phosphorylation was reversible if the animals were exposed to 48 hours of darkness after LED light treatment. All this results indicates the role of oxidative stress and the putative role of Rho phosphorylation/dephosphorylation event.

Conclusions : LP constitutes a growing problem worldwide; the consequences may have strong impact on the vision of future generations. The working model presented in this paper provides a useful tool to study specific events associated with RD under conditions of LED exposure.

This is an abstract that was submitted for the 2018 ARVO Annual Meeting, held in Honolulu, Hawaii, April 29 - May 3, 2018.

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