బయోకెమిస్ట్రీ & ఫిజియాలజీ: ఓపెన్ యాక్సెస్

నైరూప్య

Prevention of Peroxide-Induced Biochemical Damage to the Neural Retina by Caffeine: A Preliminary Report

Hegde Kavita R and Brown Destiny D

Oxidative stress is one of the significant factors in the pathogenesis of several retinal diseases, viz. age-related macular degeneration, diabetic retinopathy, etc. Available treatments are not fully effective in attenuating tissue damage and the associated vision loss. Hence development of newer therapeutic compounds is highly desirable. We have previously demonstrated the effectiveness of metabolic and nutritional antioxidants such as pyruvate and caffeine in preventing oxidative damage to the lens. However, so far, studies investigating the protective effect of caffeine on the neural retina exposed to direct oxidative stress are lacking. The primary goal of this study was therefore to examine the efficacy of caffeine in preventing biochemical damage to the neural retina exposed to oxyradicals, in terms of maintaining the concentration of glutathione (GSH), a major endogenous antioxidant reserve. In vitro short-term tissue culture studies were conducted using freshly isolated neural retinas exposed to H₂O₂ in a medium with/without caffeine supplementation. Bovine neural retinas were incubated in medium 199 for 4 hours. Oxidative stress was induced by incubating the tissue with 9 mM H₂O₂. Caffeine group was incubated with 9 mM H₂O₂⁺ caffeine (5mM). Controls were incubated without H₂O₂ and caffeine. Tissue damage was assessed by measuring GSH content following incubation. Incubation of neural retina with H₂O₂ decreased GSH level to ~40% of the controls. Caffeine, however, maintained it at ~95% of the controls, indicating its effectiveness in preventing retinal oxidative stress. This novel effect of caffeine in the neural retina has been shown for the first time. The results are highly encouraging with regard to pursuing further studies investigating its other possible mechanisms of action, and its potential neuroprotective effect.