RESUMO
Free radical formation and oxidative stress might play an important role in the pathogenesis of Parkinson's disease [PD]. In vitro data indicate that neuromelanin [NM] pigment is formed the excess cytosolic catecholamine that is not accumulated into synaptic vesicles via the vesicular monoamine transporter 2 [VMAT2]. We designed this study to investigate the neuroprotective effects of vitamin E in the early model of PD. Male rats [n = 40] with unbiased rotational behavior were randomly divided into five groups: sham operated group [SH, n = 8], vehicle-treated SH group [SH + V, n = 8], vitamin E-treated SH group [SH + E, n = 8], vehicle-treated lesion group [L + V, n = 8] and vitamin E-treated lesion group [L + E, n = 8]. Unilateral intrastriatal 6-hydroxydopamine [12.5 micro l] lesioned rats were treated intramuscularly with alpha-tocopherol acid succinate [24 I.U/kg, intramuscular [i.m.]] 1 h before surgery and three times per week for 2 month post-surgery. To evaluate the vitamin E pretreatment efficacy, tyrosine hydroxylase [TH] immunoreactivity and immunostaining intensity [ISI] for monoamine transporter 2 were used. TH immunohistochemical analyses showed a reduction of 20% in locus coeruleus [LC] cell number of vitamin E pretreated lesioned group but the cell number dropped to 60% in the lesioned group. The ISI of the cells was measured for VMAT2 in LC. Lesioned groups: 1] had the lowest VMAT2 ISI of all neurons; 2] There was an inverse relationship between VMAT2 ISI and NM pigment in the locus and 3] Neurons with the highest VMAT2 ISI also had high TH ISI. The data support the hypothesis that repeated i.m. administration of vitamin E exerts a protective effect on the LC neurons in the early model of PD