Development of the late diabetic complications is closely related to the duration and metabolic compensation of the disease. Nevertheless, a considerable interindividual variability in the development, progression and clinical extent of the late complications is observed among diabetics. Part of this variability could be ascribed to genetic factors. Considering the apparent role of glycoxidation in the pathogenesis of diabetic complications, genes encoding antioxidant enzymes modulating the overall level of oxidant stress seem to be logical candidates. Less functional variants decreasing antioxidant capacity could act pathologically during the long period of hyperglycemia-driven enhanced formation of reactive oxygen species in diabetes. The aim of the study is to examine possible associations between genetic polymorphisms in genes encoding antioxidant enzymes and other related substances (paraoxonase, NAD(P)H: quinon oxidoreductase, glyoxalase and HFE protein) and the extent of diabetic lat

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