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Abstract
The present study was undertaken to determine the effect of combination of selenium and vitamin E on experimentally induced dyskinesia in rats. The dyskinetic syndrome was produced in 4 groups of 6 male rats each weighing 250-300g by intraperitoneal (ip) administration of iminodipropionitrile (IDPN) in doses of 100m/kg body weight daily for 12 days. A group of 6 rats (group 1) served as control and received normal saline only. The rats in group 2 (IDPN only) received normal saline (ip) 30 minutes before the administration of IDPN. The animals in groups 3, 4 and 5 received selenous acid (5 μmol/kg). vitamin E (500mg/kg p.0.) and a combination of selenous acid and vitamin E respectively, daily, 30 minutes before IDPN for 12 days. Twenty four hours after the last dose of IDPN, the dyskinetic behavior including vertical head movements (retrocollis), horizontal head movements (laterocollis), circling and backwalking of each rat was studied for a period of 10 minutes. Immediately after behavioral studies, the animals were sacrificed and brains were dissected out for the analysis of conjugated dienes, lipid hydroperoxides and vitamin E. The results of this study showed that treatment of rats with IDPN only for 12 days produced dyskinetic syndrome in all the rats characterized by vertical and horizontal head movements, circling and backwalking. Concomitant treatment of rats with vitamin E and selenium individually reduced IDPN induced dyskinesia, and the symptoms were almost completely absent when the combination of these two agents was used. Our biochemical studies showed that IDPN produced a significant increase in conjugated dienes and lipid hydroperoxides and decrease in a-tocopherol in the brain of the rats, suggesting the role of free radicals in IDPN induced dyskinesia. Administration of vitamin E and or selenium protected the animals against IDPN induced lipid peroxidation in brain tissues. The results are discussed in relation to the beneficial effects of antioxidants in IDPN neurotoxicity.