1-Methyl-4-phenylpyridinium (MPP+) increases oxidation of cytochrome-b in rat striatal slices.
1-Methyl-4-phenylpyridinium (MPP+) increases oxidation of cytochrome-b in rat striatal slices.
复制标题
1-甲基-4-苯基吡啶鎓 (MPP ) 会增加大鼠纹状体切片中细胞色素-b 的氧化。
DOI：
10.1016/0006-8993(88)91611-3
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发表时间：
1988
期刊：
影响因子：
2.9
通讯作者：
Rosenthal,M
中科院分区：
文献类型：
--
作者：
Sanchez-Ramos,JR;Hollinden,GE;Sick,TJ;Rosenthal,M
采用扫描分光光度法研究了神经毒素1-甲基-4-苯基-1,2,3,6-四氢吡啶的活性代谢物1-甲基-4-苯基吡啶对大鼠纹状体切片线粒体细胞色素还原/氧化活性的影响。目的是验证神经毒素改变线粒体呼吸链中电子传递的假设。MPP+ (1 μM)对大鼠纹状体片的孵育产生了细胞色素-b的时间依赖性氧化，这与烟酰胺腺嘌呤二核苷酸（NAD）和细胞色素-b之间的线粒体内呼吸链中电子传递阻滞的概念一致。与强效多巴胺摄取抑制剂（mazindol）共孵育或在低多巴胺能神经支配的组织（海马）中研究时，MPP+的这种作用减弱。细胞色素氧化的幅度比MPP+对多巴胺能神经元的选择性作用所预期的要大，这表明MPP+对多巴胺能末端的影响继发于邻近细胞。
Effects of 1-methyl-4-phenylpyridinium, (the active metabolite of the neurotoxin, 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine), on reduction/oxidation activity of mitochondrial cytochromes were studied in rat striatal slices using scanning spectrophotometry. The objective was to test the hypothesis that the neurotoxin alters electron transport in the mitochondrial respiratory chain. Incubation of rat striatal slices with MPP+ (1 μM) produced a time-dependent oxidation of Cytochrome-bin a manner consistent with the concept of a block in electron transport in the intramitochondrial respiratory chain between nicotinamide adenine dinucleotide (NAD) and Cytochrome-b. This effect of MPP+ was decreased by co-incubation with a potent dopamine uptake inhibitor (mazindol), or when studied in a tissue with low dopaminergic innervation (hippocampus). The amplitude of Cytochrome-boxidation was greater than that expected from a selective effect of MPP+ on dopaminergic neurons suggesting that neighboring cells are influenced secondary to the MPP+ effect on dopaminergic terminals.