MPTP에 의해 유도된 Parkinsonism에 대한 selenium의 보호효과와 그 보호작용에 대한 항산화적 해독기전을 조사하기 위하여 MPTP 10mg/kg을 6일간 주사하고 selenium (25, 50, 100 ${mu}g/kg$)을 10일간 경구 투여하였으며 처음 6일간은 selenium와 MPTP를 병용 투여하였다. 실험동물을 마지막으로 selenium을 투여하고 24시간 후에 치사시켜 일반적인 독성과 항산화 방어능과 관련된 지표성분과 monoamine oxidase와 같은 신경생화학적인 지표성분들을 뇌조직에서 측정하였으며 그 결과 다음과 같은 결론을 얻었다. 우선 MPTP를 투여함에 따라 운동능력이 저하되던 것이 selenium을 투여함에 따라 운동능력이 증가되었으며, 이러한 결과의 기전은 selelnium을 투여함으로써 MPTP를 $MPP^+$로 대사시키는 MAO-B의 활성을 억제하였으며 $MPP^+$에 의해 유도된 신경독성에 대한 selenium의 보호 효과는 selenium을 투여함으로써 활성산소 해독계인 SOD, catalase, glutathione peroxidase의 활성을 증가시키기 때문인 것으로 사료된다.
This study is investigated the effect of selenium against neurotoxicity induced by MPTP(1-methy-4-phenyl-propion-oxypiperidine) in mice. In order to demonstrate neuroprotective activity of selenium, mice were administrated orally with selenium(25, 50, 100 ${mu}g/kg$, once/day) for 10 days, and MPTP(10 mg/kg) was injected subcutaneously into the mice for 6 days from the beginning 1hr before selenium treatment. Test of rota road activity was inhibited by treatment with selenium in MPTP-induced neurotoxicity group when compared to MPTP treatment group in normal mice. Monoamine oxidase(MAO)-B activity and cerebral lipid peroxide content were significantly decreased in the treatment of selenium in MPTP-induced neurotoxicity group when compared to MPTP treatment group in normal mice and MAO-A was not affected. Activities of cerebral superoxide dismutase, catalase and glutathione peroxidase were significantly increased in the treatment of selenium in MPTP-induced neurotoxicity group when compared to MPTP treatment group in normal mice. These results suggest that selenium might be estimated the result from the cooperative action of its inhibitory effect on monoamine oxidase-B with that of the enhancement of antioxidant(SOD, catalase, GSH-Px) defence ability.
