April 2010
Volume 51, Issue 13
Free
ARVO Annual Meeting Abstract  |   April 2010
Modulation of Toxic Effects of High Glucose on Retinal Cells Using Omega-3-Rich Marine Oils
Author Affiliations & Notes
  • M. Dutot
    Toxicology, YSLAB, Paris, France
  • V. de La Tourrette
    Toxicology, Faculté de Pharmacie - Université Paris Descartes, Paris, France
  • R. Fagon
    Research & Development, YSLAB, Quimper, France
  • P. Rat
    Toxicology, Faculté de Pharmacie - Université Paris Descartes, Paris, France
  • Footnotes
    Commercial Relationships  M. Dutot, YSLAB, F; V. de La Tourrette, None; R. Fagon, Yslab, E; P. Rat, None.
  • Footnotes
    Support  Adebiopharm ER 67
Investigative Ophthalmology & Visual Science April 2010, Vol.51, 5599. doi:
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      M. Dutot, V. de La Tourrette, R. Fagon, P. Rat; Modulation of Toxic Effects of High Glucose on Retinal Cells Using Omega-3-Rich Marine Oils. Invest. Ophthalmol. Vis. Sci. 2010;51(13):5599.

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

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Abstract

Purpose: : Diabetic retinopathy is characterized by an increase in oxidative stress and inflammation in the retina. In this study, we first investigated the cellular effects of high glucose on retinal pigmented epithelial (RPE) cells and Müller glial cells. Second, we focused our attention on formulations able to inhibit the toxic effects of high glucose.

Methods: : RPE cells (ARPE-19 human cell line) and Müller cells (MIO-M1 human cell line) were incubated with normal (5mM) glucose or high (25mM) glucose for 48 hours. Reactive oxygen species (ROS) production, succinate deshydrogenase activity, mitochondrial transmembrane potential, IL-6, TNFα and MCP-1 releases were evaluated using the fluorometric H2DCF-DA test, the colorimetric MTT test, the fluorometric JC-1 test and ELISA kits, respectively. Omega-3 fatty acids rich-marine oils were tested for their ability to inhibit oxidative stress and inflammation induced by high glucose.

Results: : High glucose induced ROS overproduction (+132%) and TNFα release (+376%) on RPE cells, and a decrease in succinate deshydrogenase activity (-15%), alterations of mitochondrial transmembrane potential (-35%), IL-6 and MCP-1 releases (+186% and +128%, respectively) on Müller cells. Preincubation of the cells with fish and microalgae oils, rich in EPA and/or DHA, decreased oxidative stress and inflammation, restored succinate deshydrogenase activity and mitochondrial transmembrane potential.

Conclusions: : High glucose caused increased oxidative stress, mitochondrial damages and proinflammatory cytokines release in RPE and Müller cells. Our marine formulations rich in omega-3 fatty acids are able to protect retinal cells against side effects of high glucose. Therefore, they represent an interesting therapeutic strategy for treating diabetic retinopathy.

Keywords: oxidation/oxidative or free radical damage • inflammation • nutritional factors 
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