April 2011
Volume 52, Issue 14
Free
ARVO Annual Meeting Abstract  |   April 2011
Activation Of Antioxidant Defense Mechanisms By Docosahexaenoic Acid And Eicosapentaenoic Acid Prevents Apoptosis Of Retina Photoreceptors
Author Affiliations & Notes
  • Nora P. Rotstein
    UNS-CONICET, Instituto de Investigaciones Bioquimicas, Bahia Blanca, Argentina
  • Daniela L. Agnolazza
    UNS-CONICET, Instituto de Investigaciones Bioquimicas, Bahia Blanca, Argentina
  • Luis E. Politi
    UNS-CONICET, Instituto de Investigaciones Bioquimicas, Bahia Blanca, Argentina
  • Martin-Paul G. Agbaga
    Cell Biology,
    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 112-200801-02105, PGI UNS 24ZB26, FONCyT PICT 711 (Argentina); NIH (EY00871, EY04149, EY12190, RR17703), Foundation Fighting Blindness, Research to Prevent Blindness, Hope for Vision (USA)
Investigative Ophthalmology & Visual Science April 2011, Vol.52, 5453. doi:
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    • Get Citation

      Nora P. Rotstein, Daniela L. Agnolazza, Luis E. Politi, Martin-Paul G. Agbaga, Robert E. Anderson; Activation Of Antioxidant Defense Mechanisms By Docosahexaenoic Acid And Eicosapentaenoic Acid Prevents Apoptosis Of Retina Photoreceptors. Invest. Ophthalmol. Vis. Sci. 2011;52(14):5453.

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

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Abstract

Purpose: : Oxidative stress is involved in activating the apoptosis of photoreceptors (PHRs) in several retinal neurodegenerative diseases. We have shown that docosahexaenoic acid (DHA), the major polyunsaturated fatty acid in the retina, protects PHRs from apoptosis induced by the oxidant paraquat (PQ) by activating the ERK pathway. Here we investigated if DHA metabolic precursor, eicosapentaenoic acid (EPA), had a similar protective effect and if this protection involved the activation of antioxidant defense mechanisms in PHRs.

Methods: : Rat retina neuronal cultures were supplemented with EPA, DHA, palmitic, oleic or arachidonic acids. Oxidative stress was induced at day 3 with PQ or hydrogen peroxide (H2O2). Apoptosis was evaluated by TUNEL and DAPI labeling and cell death by propidium iodide labeling. Reactive oxygen species (ROS) were measured using DCFDA and glutathione peroxidase activity was determined. Fatty acid composition of cultures supplemented with or without EPA was evaluated by GLC.

Results: : EPA and DHA protected PHRs from PQ-induced apoptosis, while other fatty acids had no protective effect. Analysis of the fatty acid composition of neurons supplemented with EPA revealed EPA levels remained constant while DHA content significantly increased compared to controls. H2O2 treatment induced PHR apoptosis and increased ROS production. DHA and EPA prevented H2O2-induced apoptosis, simultaneously decreasing ROS formation. Analysis of enzymatic activity evidenced that DHA addition increased glutathione peroxidase activity in cultures treated with or without H2O2.

Conclusions: : Our results show that only EPA and DHA protect PHRs from oxidative damage, and suggest that EPA protection might arise, at least partly, from its metabolization to DHA. They also imply that DHA might activate antioxidant defense mechanisms to protect PHRs from oxidative stress.

Keywords: apoptosis/cell death • lipids • photoreceptors 
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