Introduction: Parkinson\rquote s disease (PD) is a human neurodegenerative disorder which is associated with a massive and progressive degeneration of dopaminergic neurons in subistantia nigra (SN). There is a strong evidence of an oxidative stress participates in the etiology of PD.
Materials and Methods: The rats were divided into sham-operated, experimental and vitamin E-treated groups. For anesthesia, a mixture of ketamine and xylazine was used (i.p.). The experimental group received 5ml of 0.9% saline containing 6-hydroxydoppamine (6-OHDA) and 2% ascorbic acid in addition to 0.8 ml/kg of propylene glycol (PG, i.m.), and sham-operated group received and identical volume of saline- ascorbate in left side of striatum. The vitamin E-treated group received D-a-tocopheryl acid succinate (24 I.U./Kg, i.m.) dissolved in PG, one hour before the surgery and three times a week for a month after the surgery. Tyrosine hydroxylase (TH) immunohistochemistry in SN and striatum was used as an index for the tratment efficacy.
Results: The results, showed than an over all reduction (47%) in the number of TH immunoreactive (IR) neurons in the left SN-cell was observed in 6-OHDA lesioned group (P<0.005). However, the cell loss had attenuated to 18% in vitamin E-treated animals (P<0.05) compared with the right side. A non-significant difference in the number of TH-positive neurons between the sham-operated and the vitamin E-treated groups was noticed. A microscopic inspection of the injection site in the striatum revealed that in all treated animal, there was a dense halo of TH-IR fiber around the needle track. A grater loss of TH-IR fiber has been observed around the injection site in the experimental group.
Conclusion: Vitamin E-treatment can enhance the resistance and longitivity of dopaminergic nigral neurons against the oxidative stress induced by 6-OHDA. The results may prompt an interest in the use of vitamin E as a neuroprotective agent in the treatment of PD.