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Mitochondrial lipid peroxidation and superoxide dismutase in rat hypertensive target organs
T Ohtsuki1, M Matsumoto, K Suzuki
1First Department of Internal Medicine, Osaka University Medical School, Japan.
Abstract:
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.
Insights
Hypertension elevates lipid peroxidation and impairs mitochondrial function in the brain, but not the heart or kidneys. This brain-specific oxidative stress may lead to neuronal damage in hypertensive individuals.
Area of Science:
- Biochemistry
- Cardiovascular Science
- Neuroscience
Background:
- Mitochondrial respiratory chains produce superoxide radicals, leading to lipid peroxidation.
- Manganese superoxide dismutase (MnSOD) detoxifies superoxide within mitochondria.
- Hypertension is associated with oxidative stress in target organs.
Purpose of the Study:
- To investigate lipid peroxidation and MnSOD levels in the brain, heart, and kidney of hypertensive rats.
- To determine if hypertension causes abnormal mitochondrial metabolism of oxygen radicals in specific organs.
Main Methods:
- Assessed thiobarbituric acid-reactive substance (lipid peroxidation marker) and MnSOD concentration.
- Utilized spontaneously hypertensive rats and deoxycorticosterone acetate salts-induced hypertensive rats.
- Compared findings with normotensive control rats across different ages.
Main Results:
- Normotensive rats showed increased lipid peroxidation and MnSOD in the brain with maturation.
- Hypertensive rats exhibited elevated brain lipid peroxidation but no compensatory increase in MnSOD.
- No significant differences in lipid peroxidation or MnSOD were observed in the heart and kidney.
Conclusions:
- Hypertension selectively causes abnormal mitochondrial oxygen radical metabolism in the brain.
- This brain-specific oxidative stress may contribute to mitochondrial injury and neurodegeneration in hypertension.
- Findings suggest increased susceptibility to brain ischemia in mature hypertensive rats due to altered brain mitochondrial function.