Abstract
Purpose :
Oxidative stress is known to be involved in the pathogenesis of several retinal diseases such as diabetic retinopathy, age-related macular degeneration, retinitis pigmentosa, etc. Caffeine, a xanthine alkaloid, is a highly effective scavenger of reactive oxygen intermediates, and has been previously demonstrated to protect the lens against oxidative damage and consequent cataract formation. The primary objective of this study is to examine whether caffeine will be able to protect the neural retina against direct peroxide-induced biochemical stress.
Methods :
Neural retinas dissected from bovine eyes enucleated immediately after euthanization were incubated in medium 199 for 4 hours in a humidified incubator maintained at 37 degrees C and 5% CO2. Peroxide stress was induced by the addition of H2O2 to a final concentration of 9mM. The medium in the caffeine group contained 9mM H2O2 + caffeine (5mM). The control group was incubated without peroxide and caffeine. Post-incubation retinas were processed for determination of water soluble protein concentration using Bradford’s reagent. Biochemical damage was assessed by measurement of glutathione (GSH).
Results :
Exposure to H2O2 led to ~40% decrease in the level of GSH in the neural retina as compared to the controls. Addition of caffeine maintained its level to ~95% of the control value. The maintenance of GSH level by caffeine in neural retina exposed to oxidative stress was hence clearly evident.
Conclusions :
The above results suggest that caffeine is significantly effective in preventing biochemical damage to the neural retina subjected to peroxide stress. This is partly attributed to the known oxyradical scavenging effect of caffeine. Additional possible mechanisms of its protective effect, such as the modulation of expression of antioxidant genes and its role in boosting metabolism, are currently being investigated.
This is an abstract that was submitted for the 2018 ARVO Annual Meeting, held in Honolulu, Hawaii, April 29 - May 3, 2018.