Intensive stress response can play an important role in tissue injury. The mechanisms involved in these tissue injuries are still controversial. Oxygen free radicals (OFRs) are postulated to be among the causal factors. Exposure to stress could influence the development & course of diabetic complications through its effects on free radical production and the antioxidant status. The present work aimed at studying the effects of acute water immersion restraint (WIR) stress on lipid peroxidation measured as thiobarbituric acid reactive substances (TBARS) and the antioxidants superoxide dismutase (SOD), glutathione (GSH) and vitamin E in the heart & kidney tissues of normal and diabetic rats. The effects of stress on plasma glucose and catecholamines were also assessed. Thirty-two adult male rats were included in the study. They were divided into 4 groups: Group I (controls), Group II (stressor exposed), Group III: Diabetic rats, Group IV: (Diabetic rats & stressor exposed). The diabetic state was associated with increased SOD activity and decreased vitamin E level in the heart & kidney tissues compared to controls. Also, a decreased level of GSH was found in the kidney of diabetic rats. Because of these changes in the antioxidant system, diabetic tissues resisted lipid peroxidation as indicated by significant decrease in TBARS in the heart while their levels tended to decline in the kidney tissue compared to controls. Diabetic rats had higher basal catecholamines & showed enhanced stress response as evidenced by the higher plasma catecholamines level after stress compared to non-diabetic stressed rats. Exposure of non-diabetic rats to acute WIR stress resulted in compensatory increase of GSH level & SOD activity as well as a decrease of vitamin E level in the heart & kidney tissues compared to controls. As a result, the levels of TBARS were significantly decreased in the heart whereas, in the kidney, a slight non-significant decline was detected. However, on exposure of diabetic rats to acute WIR stress, the levels of TBARS were significantly increased in their heart & kidney tissues despite the compensatory increase of SOD activities in the heart & kidney as well as increased GSH & decreased vitamin E levels in the kidney compared to non-stressed diabetic rats. In conclusion: Stress promoted increased oxidative injury in tissues of diabetic rats and may favor of the development of diabetic complications. Therefore, if the results on experimental animals could be extended to humans, it is recommended that the diabetic patients, besides avoiding the stress, should be instructed to take antioxidants.