Prevention of Oxidative Stress-induced Metabolic Aberrations in the Neural Retina by Caffeine

Abstract

Oxyradical-induced damage to the retina has been implicated as one of the contributing factors in the pathogenesis of vision-impairing diseases such as diabetic retinopathy (DR) and age-related macular degeneration (AMD). It is hypothesized that caffeine, a nutraceutical antioxidant, will be effective in preventing metabolic aberrations in the neural retina exposed to oxygen radicals. This hypothesis is based on our previous studies demonstrating its effectiveness in preventing oxidative damage to the lens, and in protecting the neural retina against UV-A- and peroxide-induced biochemical damage. Bovine neural retinas were incubated in medium 199 at 37°C for 6 hours. Xanthine (XA)-xanthine oxidase (XO) were used to generate reactive oxygen species (ROS). Incubations were conducted in 3 groups- control, experimental (with XA+XO), and caffeine group (XA + XO+ 5mM caffeine). Retinas were then processed for determining protein, lactate and pyruvate concentrations. Lactate concentration in the controls was 2.62±0.43mM/mg protein, decreasing to 1.04±0.3 mM/mg protein in the presence of XA+XO. Its level in the caffeine group was significantly higher, 2.44±0.65 mM/mg protein, close to the controls. Pyruvate concentration in the controls was 0.16±0.05mM/mg protein, which declined significantly with XA+XO to 0.066±0.02 mM/mg protein. Such decrease was substantially prevented in the caffeine group, wherein its concentration was 0.156±0.03mM/mg protein. Caffeine was thus found to be highly effective in preventing metabolic aberrations, due to its ability to scavenge oxyradicals and thereby possibly prevent inactivation of key enzymes. Such effect of caffeine in maintaining metabolism of the neural retina exposed to ROS has been shown for the first time.