Mitochondrial enzyme activities as
biochemical markers of aging

Navarro A.
Department of Biochemistry
and Molecular Biology,
Faculty of Medicine,
University of Cadiz,
11003 Cadiz, Spain.
2004 Feb-Apr;25(1-2):37-48.


The decrease of neurological performance in normal aging is directly related to brain oxidative stress and inversely related to lifespan. Male mice lifespan was increased by 8-10% (median and maximal lifespan, respectively) in mice with high spontaneous neurological activity, by 21-15% after moderate exercise; and by 25-20% after supplementation with vitamin E. Oxidative stress markers, TBARS and protein carbonyl content, were found increased on aging; a higher content of oxidation products is considered an effective aging factor, specially in the brain, with a majority of postmitotic cells. Mitochondrial enzyme activities, mitochondrial nitric oxide synthase (mtNOS), NADH dehydrogenase and cytochrome oxidase, behaved as markers of brain aging. The decrease in enzyme activities was directly related to the content of oxidation products and to the loss of neurological function in aged mice, this latter was determined in the tighrope and the T-maze tests. The above mentioned conditions that increased mice lifespan were effective to decrease the level of oxidative stress markers, and to retard the decreases in mitochondrial enzyme activities and neurological function associated to aging. The activities of mtNOS, NADH dehydrogenase and cytochrome oxidase may be used as indicators of the effectiveness of antiaging treatments.

Caloric restriction
Intermittent fasting
Antiaging medicine?
Antiaging treatments
Antagonistic pleiotropy
Caloric restriction mimetics
Cryonics/negligible senescence
Lifespan-extending interventions
CR/age-related oxidative damage

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