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Peter J. Hornsby, PhD
Department of Cell and Molecular Biology Medical College of Georgia Augusta, GA 30912

Arch Neurol. 1989;46(8):840-841.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

To the Editor.

—1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) causes parkinsonism in humans and experimental animals by causing the death of dopaminergic striatal neurons. The ultimate toxin is thought to be a monoamine oxidase metabolite of MPTP, the 1-methyl-4-phenylpyridinium ion (MPP+), which is transported by the normal dopamine reuptake system, is concentrated by the mitochondria, and then poisons the cell by blocking the respiratory chain.^1-3

Several authors have presented evidence for the involvement of oxygen radical damage in the toxic effects of MPTP.⁴ Dopaminergic neurons accumulate lipofuscin, a hallmark of oxidative damage, after MPTP administration.^5,6 Some experiments, although not all, have demonstrated amelioration of MPTP-caused dopaminergic neuron loss by prior administration of antioxidants, including vitamin E.^2,7 Other data also demonstrate initiation of oxidative damage by MPTP in various systems.^8-10 Moreover, the possible involvement of oxidative damage in the loss of dopaminergic neurons in idiopathic Parkinson's disease has led to . . . [Full Text PDF of this Article]

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