Modulatory effects of centrophenoxine on different regions of ageing rat brain.
The debilitating consequences of age-related brain deterioration are widespread and extremely costly in terms of quality of life and longevity. Free radical induced damage is thought to be responsible, at least in part, for the degenerative effects of aging. This may be largely due to high-energy requirements, high oxygen consumption, high tissue concentration of iron and low of antioxidant enzymes in brain. Therefore, supplementing an external source of free radical scavenger would greatly benefit in ameliorating the free radical damage which may thus be beneficial in aging. In the present study, an important nootropic agent Centrophenoxine, which has an easy access to brain, has been administered to aged animals (16 months old). Rats aged 6 months (young group) and 16 months old (old group) were chosen for the study. Both groups were administered Centrophenoxine (dissolved in physiological saline) intraperitoneally once a day for 6 weeks. Our study indicates an increased activity of Catalase, Superoxide Dismutase, Glutathione reductase, as well as an increase in the reduced, oxidized, and total glutathione content thus resulting in an altered redox state. A substantial increase in the malondialdehyde content was also reported as a result of aging. Whereas, following Centrophenoxine administration (100 mg/kg body weight/day, injected i.p) alterations in the activities of Superoxide dismutase, Glutathione reductase as well as in the reduced and oxidized glutathione content was reported in aged rat brain. Lipid peroxidation was also reported to be significantly decreased in aged animals after Centrophenoxine supplementation for 6 weeks. The use of an extraneous antioxidant substance may prove beneficial in combating the conditions of oxidative stress in ageing brain.
Bhalla
Punita
P
Department of Biophysics, Panjab University, Chandigarh 160 014, India.
Nehru
Bimla
B
D000375:Aging; D000818:Animals; D001921:Brain / Q000187:drug effects / Q000378:metabolism*; D002374:Catalase / Q000378:metabolism; D002531:Cerebellum / Q000187:drug effects / Q000378:metabolism; D005260:Female; D005978:Glutathione / Q000378:metabolism; D005980:Glutathione Reductase / Q000378:metabolism; D007031:Hypothalamus / Q000187:drug effects / Q000378:metabolism; D008049:Lipase / Q000378:metabolism; D015227:Lipid Peroxidation / Q000187:drug effects; D002504:Meclofenoxate / Q000494:pharmacology*; D008526:Medulla Oblongata / Q000187:drug effects / Q000378:metabolism; D018696:Neuroprotective Agents / Q000494:pharmacology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D013482:Superoxide Dismutase / Q000378:metabolism; D013687:Telencephalon / Q000187:drug effects / Q000378:metabolism
D018696:Neuroprotective Agents; D002504:Meclofenoxate; D002374:Catalase; D013482:Superoxide Dismutase; D005980:Glutathione Reductase; D008049:Lipase; D005978:Glutathione