Abstract
Nonenzymatic glycosylation of lens proteins in diabetes mellitus is one of the pathogenetic mechanisms of cataract formation. According to the results of this study, aminoguanidine, which has anti-glycation activity, inhibits cataractogenesis in experimental diabetes. Laboratory animals with streptozotocin-induced diabetes mellitus treated with aminoguanidine showed less clouding in the lenses, and the content of advanced glycation end products, in particular, carboxymethyllysine, in the lenses was found to be reduced compared to the same parameters in animals from the control diabetic group.
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