MITOCHONDRIAL LIPID-PEROXIDATION AND SUPEROXIDE-DISMUTASE IN RAT HYPERTENSIVE TARGET ORGANS

Mitochondrial respiratory chains leak a large amount of superoxide anion radicals, which chain react with membrane phospholipid to develop lipid peroxidation. Manganese superoxide dismutase (MnSOD) is then inducible and catalyzes superoxide detoxification within mitochondria. We examined mitochondrial thiobarbituric acid-reactive substance, an end product of lipid peroxidation, and MnSOD concentration in hypertensive target organs of spontaneously hypertensive and deoxycorticosterone acetate salts-induced hypertensive rats. Normotensive rats showed significant increases in thiobarbituric acid-reactive substance and MnSOD in the brain as they matured. Mature spontaneously hypertensive and induced hypertensive rats showed a marked elevation of lipid peroxidation but no increase in superoxide dismutase in the brain. The heart and kidney presented no significant difference of lipid peroxidation and superoxide dismutase among strains, ages, and treatments. Abnormal mitochondrial metabolism of oxygen radicals was observed selectively in the brain during hypertension and may contribute to mitochondrial injury and lead to neuronal degeneration or susceptibility to brain ischemia in mature hypertensive rats.