Hepatospecific signs of disorders in the free radical oxidation-antioxidation defense system in rats with diabetes mellitus aggravated by cerebral ischemia-reperfusion

Abstract

Cerebral hypoxia results in considerable pathological-histological changes in the internal organs with disorders of their functional state. In case of diabetes mellitus metabolic disorders cause liver damage as well, therefore diabetes aggravated by cerebral ischemia-reperfusion should logically make morphofunctional changes in this organ worse.Objective of the study: to examine the signs of oxidative and nitrosative stress in the liver of rats with diabetes mellitus aggravated by cerebral ischemia-reperfusion.Material and methods. The content of the products of lipid peroxide oxidation, oxidative protein modification, metabolites of nitrogen oxide and activity of antioxidant enzymes were investigated in the liver homogenates of rats. Diabetes mellitus was simulated by means of a single intraperitoneal injection of streptozotocin (Sigma, USA, 60 mg/kg). The results were assessed after 20-minute carotid ischemia with one hour reperfusion and on the 12th day of post-ischemic period. Results. According to the changes in the content of lipid peroxidation products and activity of antioxidant enzymes 20-minute carotid ischemia with one hour reperfusion results in the depression in the lipoperoxidation-antioxidation defense system. On the 12th day of the experiment the content of diene conjugates in this organ increases against the background of an increased activity of superoxide dismutase and glutathione peroxidase which, in general, is indicative of a compensatory character of the reaction of the lipid peroxidation-antioxidant defense system. The indices of oxidation protein modification and nitrogen oxide metabolism during the early post-ischemic period remain without changes in the liver of animals from this group, and they increase on the 12th day of the experiment, which is indicative of the availability of oxidative and nitrosative stress during this period. In the liver of animals with diabetes mellitus the reaction of all the mentioned indices is absent both during early and late post-ischemic periods. Conclusion. The lack of the signs of lipid peroxidation, protein oxidative modification, nitrogen oxide metabolism and activity of antioxidant defense in the liver of animals with diabetes mellitus both during early and late post-ischemic periods is indicative of areactivity of these biochemical indices concerning cerebral ischemia-reperfusion.