the neuroprotive effects of vitamin e on nigral neurons after lesioning by 6-hydroxydopamine in the rat: an immunohistochemical study of tyrosine hydroxyase

introduction: parkinsonrquote 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.