neotetrazolium and Brain-Ischemia

We analyzed the effects of S-adenosyl-L-methionine (SAM) on tissue oxidative status in a combined model of permanent focal ischemia and global reperfusion in the rat brain. The production of thiobarbituric acid reactive substances (TBARS) was measured under basal conditions and after induction with ferrous salt as an indicator of brain lipid peroxidation. Total, oxidized and reduced glutathione were measured as indicators of the antioxidant defense capacity of brain tissue. Mitochondrial reduction of tetraphenyl tetrazolium (TPT) was quantified morphometrically. Results obtained in vitro showed that incubation with SAM reduced lipid peroxidation, with a maximum inhibition of 65.12+/-5.99% after incubation with 1 mmol/l; glutathione production was not significantly modified. In the brain ischemia-reperfusion model, TBARS production increased and glutathione content decreased, and mitochondrial reduction of TPT decreased significantly after ischemia-reperfusion in areas dependent on carotid circulation. The administration of 50 mg/kg SAM per day for 3 days led to the inhibition of brain lipid peroxidation and increased total glutathione production. These changes were accompanied by an increase in mitochondrial capacity to reduce TPT. We conclude that SAM reduces oxidative damage in the rat brain in an experimental model of ischemia-reperfusion.

Topics: Animals; Brain; Brain Ischemia; Glutathione; Lipid Peroxides; Male; Mitochondria; Oxidation-Reduction; Oxidative Stress; Rats; Rats, Wistar; Reperfusion Injury; S-Adenosylmethionine; Tetrazolium Salts; Thiobarbituric Acid Reactive Substances

The antioxidant effect of alpha-tocopherol was assessed in a model of ischemia-reperfusion in the rat brain. In this model, permanent ischemia of the cortical branches of the middle cerebral artery was combined with bilateral occlusion of the common carotid arteries for 1 h and restoration of circulation for a period of 2 h. Lipid peroxidation and mitochondrial reduction of tetraphenyl tetrazolium (TPT) were determined in both untreated and d-alpha-tocopherol treated rats. Ferrous sulfate and ascorbic acid (FeAs) were used to induce lipid peroxidation via the formation of hydroxyl anions. Malondialdehyde (MDA) increased in the ischemia-reperfusion areas (+101%), but FeAs-induced MDA did not vary in the area of permanent ischemia. Brain tissue undergoing ischemia-reperfusion was about 50% less sensitive to the antioxidant effect of ascorbic acid. The reduction of TPT showed 52% mitochondrial damage in the area of ischemia-reperfusion, whereas mitochondrial activity in the area of permanent ischemia was 177 times lower as compared to controls. d-alpha-tocopherol caused a 40% inhibition of MDA production and 16.5% and 21.5% decrease in mitochondrial activity in the areas of ischemia-reperfusion and permanent ischemia, respectively.

Topics: Animals; Brain; Brain Ischemia; Lipid Peroxides; Male; Malondialdehyde; Mitochondria; Oxidation-Reduction; Rats; Rats, Wistar; Tetrazolium Salts; Vitamin E