氧化氮在MPTP神經毒理作用中所扮演的角色
Date Issued
1999
Date
1999
Author(s)
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DOI
882314B002288
Abstract
Methyl-4-phenyl- 1,2,3 ,6-tetrahydropyridine (MPTP) is known to produce parkinsonism in humans and monkeys. Our previous studies have shown that MPP induced dopamine depletion and hydroxyl radicals formation and lipid peroxidation in the striatum of rats. Recent reports have suggestec. that MPTP toxicity could be prevented by 7-nitroindazole (7-NI, a potent inhibitors of neuronal nitric oxide synthase). It is suggested that MPP may interfere with mitochondrial electron transport and result in a leakage of superoxide anion. Nitric oxide (N0), produced following activation of N-methyl-D-aspartate (NM JA) receptors, combined with superoxide to form the toxic free radical peroxynitrito, which in turn may degenerate into more noxious hydroxyl radical and cause cell damage. However, evidence suggested that another nitric oxide synthase (NOS) inhibitor, L-N¢X nitro arginine methyl ester (L-NAME, another NOS inhibitor) did not show protection against MPTP-induced toxicity in the marmoset. Using the IvIPTP-Parkinsonism model, the present study showed that both of 7-NI and L-NAME did not exert protective on
dopaminergic neurons in term of the inhibition of dcpamine depletion and hydroxyl radical formation induced by MPP in the striatum.
Subjects
MPTP
nitric oxide
Parkinsonism
7-nitroindazole
L-NG nitro arginine methyl ester
microdialysis
Publisher
臺北市：國立臺灣大學醫學院神經科
Type
journal article
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