Dietary Docosahexaenoic Acid (DHA) Protects Retinal Function Against Ischemia–Reperfusion in the Rat

Abstract

Purpose: : The purpose of this study was to evaluate the effectiveness of dietary omega–3 polyunsaturated fatty acids (PUFA) to prevent the consequences of ischemia–reperfusion on retinal function in the rat.

Methods: : Wistar rats were bred on omega–3 PUFA deficient diets for 2 generations. The third generation of animals was fed either with the same deficient diet or re–nourished with a control diet containing alpha linolenic acid (ALA) as the sole source of omega–3 PUFA (ALA group) or a diet supplemented with DHA (0.8% of total lipids, DHA group). After 14 months of feeding, retinal ischemia was induced for 60 minutes in the right eye by raising intraocular pressure to 110 mm Hg by canulation of the anterior chamber. After 7 days of reperfusion, the scotopic ERG was recorded on both eyes. Retinal lipids were extracted and analyzed by gas chromatography.

Results: : Omega–3 PUFA supplementations were able to restore retinal DHA (35.2% and 32.7% of retinal lipids in DHA and ALA groups, respectively), when compared to omega–3 PUFA deprived animals. Omega–3 supplementations resulted in higher ERG b–wave amplitudes when compared to deficiency (555 µV, 475 µV and 414 µV in DHA, ALA and deficient groups, respectively). However, only ALA supplementation resulted in higher a–wave amplitudes (74 µV, 47 µV and 46 µV in ALA, DHA and deficient groups, respectively). When compared to the fellow eye, ischemia–reperfusion reduced scotopic b– and a–wave amplitudes of the treated eye by 48.5% and 61.8% in deficient rats whereas the reduction was limited to 24.7% and 67.6% in animals from ALA group and to 8.9% and 40.1% in those from DHA group.

Conclusions: : Both ALA and DHA were able to restore DHA levels in the retina. In this experimental setting, DHA was the most effective to protect the retina against ischemia/reperfusion–induced ERG alterations.

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