百草枯、1-甲基-4-苯基吡啶离子及其类似物生物还原的模型研究。关于1-甲基-4-苯基-1,2,3,6-四氢吡啶神经毒性中“氧化还原循环”机制的反证。
Model study on the bioreduction of paraquat, MPP+, and analogs. Evidence against a "redox cycling" mechanism in MPTP neurotoxicity.
作者信息
Frank D M, Arora P K, Blumer J L, Sayre L M
机构信息
Department of Chemistry, Pediatrics, Case Western Reserve University, Cleveland, OH 44106.
出版信息
Biochem Biophys Res Commun. 1987 Sep 30;147(3):1095-104. doi: 10.1016/s0006-291x(87)80183-3.
The ability of paraquat, MPP+, and analogs to be reduced by chemical reductants and by NADPH, as catalyzed by liver microsomes or purified NADPH cytochrome P-450 reductase, is reported. The analogs span a range of electrochemical potential, including values in-between that of paraquat and MPP+. Analogs with an Eo below -.55 V (vs. NHE) are not reduced by either the NADPH-microsomes or NADPH-reductase systems. The inability of MPP+ to be bio-reduced or to stimulate the production of superoxide during aerobic reduction is evidence against a redox-cycling (oxidant stress) role of MPP+ in MPTP neurotoxicity.
据报道，百草枯、MPP⁺及其类似物可被化学还原剂以及在肝脏微粒体或纯化的NADPH细胞色素P-450还原酶催化下被NADPH还原。这些类似物涵盖了一系列电化学势，包括介于百草枯和MPP⁺之间的值。Eo低于-0.55 V（相对于标准氢电极）的类似物不能被NADPH-微粒体或NADPH-还原酶系统还原。MPP⁺不能进行生物还原或在有氧还原过程中刺激超氧化物的产生，这证明MPP⁺在MPTP神经毒性中不存在氧化还原循环（氧化应激）作用。
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