March 2012
Volume 53, Issue 14
Free
ARVO Annual Meeting Abstract  |   March 2012
Eicosapentaenoic Acid Is Metabolized To Docosahexaenoic Acid In Retina Neurons To Protect Photoreceptors From Apoptosis Induced By Oxidative Stress
Author Affiliations & Notes
  • Nora P. Rotstein
    UNS-CONICET, Inst de Investigaciones Bioquimicas, Bahia Blanca, Argentina
  • Daniela L. Agnolazza
    UNS-CONICET, Inst de Investigaciones Bioquimicas, Bahia Blanca, Argentina
  • Luis E. Politi
    UNS-CONICET, Inst de Investigaciones Bioquimicas, Bahia Blanca, Argentina
  • Martin-Paul G. Agbaga
    Ophthalmology,
    Univ of Oklahoma Hlth Sci Ctr, Oklahoma City, Oklahoma
  • Robert E. Anderson
    Ophthalmology/Cell Biology,
    Univ of Oklahoma Hlth Sci Ctr, Oklahoma City, Oklahoma
  • Footnotes
    Commercial Relationships  Nora P. Rotstein, None; Daniela L. Agnolazza, None; Luis E. Politi, None; Martin-Paul G. Agbaga, None; Robert E. Anderson, None
  • Footnotes
    Support  PIP CONICET 112-200801-021-105, PGI UNS, 24ZB26 (NP, LP), FONCyT PICT 711 (LP) (Argentina); NIH EY04149, EY00871, and EY12190, RP; Foundation Fighting Blindness (REA);, Hope for Vision (MPA)
Investigative Ophthalmology & Visual Science March 2012, Vol.53, 4289. doi:
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    • Get Citation

      Nora P. Rotstein, Daniela L. Agnolazza, Luis E. Politi, Martin-Paul G. Agbaga, Robert E. Anderson; Eicosapentaenoic Acid Is Metabolized To Docosahexaenoic Acid In Retina Neurons To Protect Photoreceptors From Apoptosis Induced By Oxidative Stress. Invest. Ophthalmol. Vis. Sci. 2012;53(14):4289.

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

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Abstract

Purpose: : Oxidative stress triggers apoptosis of photoreceptors (PHRs) and is involved in several retinal neurodegenerative diseases. We have previously established that docosahexaenoic acid (DHA), the major polyunsaturated fatty acid in the retina, promotes PHR differentiation and protects PHRs from oxidative stress-induced apoptosis. We recently demonstrated that eicosapentaenoic acid (EPA), a DHA metabolic precursor, had a similar protective effect. We here investigated if EPA also enhanced PHR differentiation and whether it exerts its effects by itself or through its metabolization to DHA.

Methods: : Pure neuronal cultures prepared from rat retinas were supplemented with or without EPA at day 1. Desaturation of EPA was inhibited by adding CP-24879 hydrochloride, a Δ5/Δ6 desaturase inhibitor, one hour before EPA supplementation. Oxidative stress was induced at day 3 with paraquat (PQ) or hydrogen peroxide (H2O2). Differentiation was determined by analyzing opsin expression. Apoptosis was evaluated by TUNEL assay and DAPI labeling and cellular viability with propidium iodide. Mitochondrial integrity was determined with the fluorescent probe Mitotracker. Fatty acid composition of cultured neurons was evaluated by GLC.

Results: : Supplementation with EPA increased opsin expression and protected PHRs from PQ and H2O2-induced apoptosis, preserving their mitochondrial membrane potential. EPA addition did not modify EPA content in retina neurons, but significantly increased DHA levels, compared to cultures lacking EPA. Adding CP-24879 to the cultures prior to EPA supplementation prevented the increase in DHA levels, in spite of EPA addition. Moreover, inhibition of DHA synthesis completely blocked EPA protective effect on PHRs from oxidative stress-induced apoptosis.

Conclusions: : Our results suggest that EPA promoted PHR differentiation and rescued PHRs from apoptosis induced by oxidative stress through its elongation and desaturation to DHA, implying that retina neurons, at least in culture, are able to synthesize this fatty acid.

Keywords: photoreceptors • lipids • neuroprotection 
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