Dose-dependent protective effect of selenium in rat model of Parkinson's disease: neurobehavioral and neurochemical evidences
Article first published online: 13 JAN 2003
Journal of Neurochemistry
Volume 84, Issue 3, pages 438–446, February 2003
How to Cite
Zafar, K. S., Siddiqui, A., Sayeed, I., Ahmad, M., Salim, S. and Islam, F. (2003), Dose-dependent protective effect of selenium in rat model of Parkinson's disease: neurobehavioral and neurochemical evidences. Journal of Neurochemistry, 84: 438–446. doi: 10.1046/j.1471-4159.2003.01531.x
- Issue published online: 13 JAN 2003
- Article first published online: 13 JAN 2003
- Received February 12, 2002; revised manuscript received May 14, 2002; accepted August 13, 2002.
- oxidative stress;
- Parkinson's disease;
Normal cellular metabolism produces oxidants that are neutralized within cells by antioxidant enzymes and other antioxidants. An imbalance between oxidant and antioxidant has been postulated to lead the degeneration of dopaminergic neurons in Parkinson's disease. In this study, we examined whether selenium, an antioxidant, can prevent or slowdown neuronal injury in a 6-hydroxydopamine (6-OHDA) model of Parkinsonism. Rats were pre-treated with sodium selenite (0.1, 0.2 and 0.3 mg/kg body weight) for 7 days. On day 8, 2 µL 6-OHDA (12.5 µg in 0.2% ascorbic acid in normal saline) was infused in the right striatum. Two weeks after 6-OHDA infusion, rats were tested for neurobehavioral activity, and were killed after 3 weeks of 6-OHDA infusion for the estimation of glutathione peroxidase, glutathione-S-transferase, glutathione reductase, glutathione content, lipid peroxidation, and dopamine and its metabolites. Selenium was found to be successful in upregulating the antioxidant status and lowering the dopamine loss, and functional recovery returned close to the baseline dose-dependently. This study revealed that selenium, which is an essential part of our diet, may be helpful in slowing down the progression of neurodegeneration in parkinsonism.