Przedborski S, Jackson-Lewis V
Columbia University, Neurology Department, New York, NY 10032, USA.
Mov Disord. 1998;13 Suppl 1:35-8.
1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) produces an experimental model of Parkinson's disease (PD). It replicates most of the clinical features of PD as well as the main biochemical and pathologic hallmarks of the disease. Although the MPTP model departs from PD in several aspects, it is thought that important insights into the neurodegenerative process of PD may be obtained by elucidating the molecular mechanism of MPTP. In this article, we summarize the different steps of the complex metabolic pathway of MPTP and show how they may be implicated in predisposing individuals to PD. We also outline findings pertinent to the mode of action of MPTP including overproduction of free radicals, implication of nitric oxide, nitration of tyrosine, impairment of mitochondrial respiration, and occurrence of apoptosis. All of these factors may participate in the cascade of deleterious events that ultimately lead to the death of dopaminergic neurons after MPTP administration. Because of the similarity between PD and the MPTP model, we are speculating that a similar scenario may underlie the neurodegenerative process in PD.
1-甲基-4-苯基-1,2,3,6-四氢吡啶(MPTP)可产生帕金森病(PD)的实验模型。它复制了PD的大多数临床特征以及该疾病的主要生化和病理特征。尽管MPTP模型在几个方面与PD有所不同,但人们认为,通过阐明MPTP的分子机制,可能会获得对PD神经退行性过程的重要见解。在本文中,我们总结了MPTP复杂代谢途径的不同步骤,并展示了它们如何可能使个体易患PD。我们还概述了与MPTP作用方式相关的研究结果,包括自由基的过度产生、一氧化氮的影响、酪氨酸的硝化、线粒体呼吸的损害以及细胞凋亡的发生。所有这些因素可能都参与了一系列有害事件,这些事件最终导致MPTP给药后多巴胺能神经元的死亡。由于PD与MPTP模型之间存在相似性,我们推测类似的情况可能是PD神经退行性过程的基础。