RESUMO
The role of acetylation in the antiglycating and anticataract effects of aspirin (ASA) is explored by comparing ASA's effects with that of sodium salicylate (SS), a nonacetyl analog of ASA, on cataract development in diabetic rats. Streptozocin diabetic rats were provided with either ASA or SS, orally, for 24 weeks. Appropriate drug controls, normal controls and diabetic controls were run in parallel. Periodic estimations of blood glucose, glycated hemoglobin and assessments of cataract progression were done. After 24 weeks lenses were removed, homogenised and separated into water soluble fraction and urea soluble fraction. The glycated lens proteins in each fraction was quantified. Results were analysed statistically and interpreted in relation to serum salicylate levels. Both ASA and SS did not influence blood glucose levels. In the untreated diabetic groups the onset and progression of cataract was quicker and complete within 16 weeks. Both ASA and SS delayed the onset and progression in diabetic rats, but ASA's effect was more pronounced than that of SS. The levels of glycated Hb and lens proteins in diabetic rats were significantly reduced by ASA and not by SS for the same serum salicylate levels. ASA's anticataract potential far exceeds that of SS and it is ASA, and not SS, that inhibits protein glycation. Thus the results favour the hypothesis that acetylation plays a major role in ASA's anticataract effect via inhibition of glycation.