MPTP公司
神经毒素
代谢物
线粒体
化学
氧化磷酸化
生物化学
谷氨酸受体
立体化学
多巴胺
生物
内分泌学
受体
多巴胺能
作者
William J. Nicklas,I Vyas,Richard E. Heikkila
出处
期刊:Life Sciences
[Elsevier BV]
日期:1985-07-01
卷期号:36 (26): 2503-2508
被引量:1239
标识
DOI:10.1016/0024-3205(85)90146-8
摘要
1-methyl-4-phenylpyridine (MPP+), a major metabolite of the neurotoxin, 1-methyl-4-phenyl-1,2,5,6-tetrahydropyridine (MPTP) inhibited the ADP-stimulated and uncoupled oxidation of NADH-linked substrates by brain mitochondrial preparations. MPTP itself was ineffective. The apparent Ki's for MPP+ inhibition of pyruvate or glutamate oxidation by purified rat brain mitochondria were approximately 300 and 400 microM, respectively; with mouse brain mitochondria the values were lower, 60 and 150 microM, respectively. Succinate oxidation was unaffected by either compound. Compromise of mitochondrial oxidative capacity by MPP+ could be an important factor in mechanisms underlying the toxicity of MPTP.
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