Eye lens cataract can develop by various mechanisms the details of which are not completely known. Increased level of glucose in patients with diabetes mellitus represents one of the factors accelerating cataract development. As the lens does not depend on insulin, cataract formation is induced by hyperglycaemia both in IDDM and NIDDM patients. Glucose attacks free aminogroups of proteins and glycation products are formed by multistep non-enzymatic reactions. We can discriminate early and late products. The latter are often called as advanced glycation endproducts (AGE). They can accumulate inside the lens and interfere with its optical properties. With regard to the fact that glycation reactions are accompanied by autooxidation reactions, the overall process is usually referred to as glycoxidation. Free radical oxidations of membrane lipids give similar products as do glycation reactions, and there is synergy between these two pathways. Development of eye cataract is accompa- nied by a decrease in lens antioxidant capacity. A new class of glycation inhibitors has been observed recently. They are called Amadorins and they have therapeutic potential in the cataract treatment.

        Key words: cataract, hyperglycaemia, nonenzymatic glycation, autooxidation, AGE, Amadorins