Selenium partially reverses the depletion of striatal dopamine and its metabolites in MPTP-treated C57BL mice.

Oxidative stress and inflammation have been implicated in idiopathic Parkinson's disease as well as in the mouse model of this disorder induced by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). Selenium possesses both antioxidant and anti-inflammatory properties; thus we studied the effect of selenium supplementation on MPTP-induced dopaminergic neurotoxicity in mice. C57BL male mice were treated with MPTP (30 mg/kg, i.p.), daily for 4 days. Sodium selenite (Se) was administered in the doses of 0, 1, 2 and 3 mg/kg, 30 min prior to the administration of MPTP. One group of animals served as control (saline only) and another group as Se alone (3 mg/kg). The animals were sacrificed at 24 h after the last dose of MPTP. The striata were isolated and analyzed for dopamine (DA), 3,4-dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA) levels. Administration of MPTP significantly depleted striatal DA (6.78+/-0.80 microg/g) as compared to control animals (19.32+/-0.77 microg/g) which was significantly prevented by co-treatment with 3 mg/kg dose of Se (12.28+/-0.97 microg/g). MPTP caused significant reduction in striatal DOPAC but the decrease in HVA levels was not significant. Although Se dose-dependently reversed MPTP-induced decreases in DOPAC and HVA levels, these effects were statistically not significant. These findings indicate a significant impairment of dopaminergic neurotransmission by MPTP which is partially reversed by Se treatment.