Abstract
Mitochondria are known to be a rich source for the production of free radicals and, consequently, mitochondrial components are susceptible to lipid peroxidation that decreases respiratory activity. The present investigation was designed to evaluate the neuroprotective effect of Deprenyl on mitochondrial function in rats with respect to changes in the mitochondrial energy status. Intraperitoneal administration of liquid deprenyl (2 mg/kg body weight/day for a period of 15 days i.p, significantly P< 0.05) to the experimental rats of three age groups (6, 12 &18 months old) prevented the age related reduction in Tricarboxylic acid cycle enzymes (isocitrate dehydrogenase, α-ketoglutarate dehydrogenase, succinate dehydrogenase and malate dehydrogenase) and respiratory marker enzymes (NADH dehydrogenase and cytochrome-c-oxidase) in the cerebellar mitochondria. The results of the present study indicate that the overall neuroprotective effect of deprenyl is probably related to its ability to retain the energy status of cerebellum by preserving the activities of Tricarboxylic acid cycle enzymes and respiratory marker enzymes at near normalcy and/or to its free radical- scavenging capability against age related aberrations in lipid peroxidation, which is responsible for unalterable changes in neuronal membrane.
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