The present study was designated to evaluate the effect of special antidiabetic diet treatment upon oxidative stress parameters in the initial stages of the development of diabetes. Male Wistar strain rats were used as an experimental model, divided into five groups: group 1, control rats; group 2, antidiabetic diet group; group 3, rats with induced diabetes mellitus – diabetic control; group 4, rats with induced diabetes mellitus and diet food, and group 5, rats with induced diabetes mellitus and insulin treatment.A significant decrease in superoxide dismutase (SOD) and total glutathione (GSH) activities were observed in the liver of diabetic rats when compared with control animals. There was simple evidence that elevation in glucose concentration depress natural antioxidant defense such as SOD and GSH. The observed decrease in SOD activity could result from inactivation by H2O2 or by glycation of the enzyme, which have been reported to occur in diabetes. The possible source of oxidative stress in diabetes includes shifts in redox balance resulting from altered carbohydrate and lipid metabolism, increased generation of reactive oxygen species, and decreased level of antioxidant defences such as GSH and SOD. The plasma level of aminotransferases (ALT, AST), creatine kinase (CK), lactate dehydrogenase (LDH) and urea were significantly increased after induction of diabetes, in all groups under treatment. In contrast, rats fed special diet food, have shown slight different, but not significant changes. The decrease in total protein and albumin fraction may be due to microproteinuria and albuminuria, which are important clinical markers of diabetic nephro-pathy, and-/or may be due to increased protein catabolism.The findings of the present study suggest that special diet formula useful for prevention of progressive hyperglycaemia in age induced diabetes in dogs, could not restore the imbalance of cellular defence mechanism provoked by streptozotocin.