Sershen H, Reith M E, Hashim A, Lajtha A
Neuropharmacology. 1985 Dec;24(12):1257-9. doi: 10.1016/0028-3908(85)90163-7.
Administration of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP; 2 X 8 mg/kg retro-orbital) to BALB/cBy mice reduced [3H]mazindol binding to striatal membranes by 50%. Reactive oxygen derivatives have been suggested to be involved in MPTP neurotoxicity; therefore we examined the effects of ascorbic acid (an antioxidant). Ascorbic acid (100 mg/kg) given 20 min prior to MPTP administration appreciably prevented the reduction of [3H]mazindol binding. The involvement of oxidative processes in the mechanism of MPTP neurotoxicity may suggest a relationship to the etiology of Parkinson's disease, and the possible benefit of treatment with ascorbic acid.
给BALB/cBy小鼠眶后注射1-甲基-4-苯基-1,2,3,6-四氢吡啶（MPTP；2×8毫克/千克）可使纹状体膜上的[3H]吗吲哚结合减少50%。有研究表明活性氧衍生物与MPTP神经毒性有关；因此我们研究了抗坏血酸（一种抗氧化剂）的作用。在MPTP给药前20分钟给予抗坏血酸（100毫克/千克）可显著防止[3H]吗吲哚结合的减少。氧化过程参与MPTP神经毒性机制可能提示其与帕金森病病因的关系，以及抗坏血酸治疗的潜在益处。
