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Am J Physiol Regul Integr Comp Physiol 282: R985-R992, 2002; doi:10.1152/ajpregu.00537.2001
0363-6119/02 $5.00
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Vol. 282, Issue 4, R985-R992, April 2002

Behavioral dysfunction, brain oxidative stress, and impaired mitochondrial electron transfer in aging mice

Ana Navarro1, María Jesús Sánchez Del Pino1, Carmen Gómez1, Juan Luis Peralta2, and Alberto Boveris3

Departments of 1 Biochemistry and Molecular Biology and 2 Biostatistics, Faculty of Medicine, University of Cadiz, 11003 Cadiz, Spain; and 3 Laboratory of Free Radical Biology, School of Pharmacy and Biochemistry, University of Buenos Aires, 1113 Buenos Aires, Argentina

Behavioral tests, tightrope success, and exploratory activity in a T maze were conducted with male and female mice for 65 wk. Four groups were defined: the lower performance slow males and slow females and the higher performance fast males and fast females. Fast females showed the longest life span and the highest performance, and slow males showed the lowest performance and the shortest life span. Oxidative stress and mitochondrial electron transfer activities were determined in brain of young (28 wk), adult (52 wk), and old (72 wk) mice in a cross-sectional study. Brain thiobarbituric acid reactive substances (TBARS) were increased by 50% in old mice and were ~15% higher in males than in females and in slow than in fast mice. Brain Cu,Zn-superoxide dismutase (SOD) activity was increased by 52% and Mn-SOD by 108% in old mice. The activities of mitochondrial enzymes NADH-cytochrome c reductase, cytochrome oxidase, and citrate synthase were decreased by 14-58% in old animals. The cumulative toxic effects of oxyradicals are considered the molecular mechanism of the behavioral deficits observed on aging.

neuromuscular impairment; NADH-cytochrome c reductase


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