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自由基在摇头丸诱导的小鼠神经毒性中的作用。

Involvement of free radicals in MDMA-induced neurotoxicity in mice.

作者信息

Cadet J L, Thiriet N, Jayanthi S

机构信息

Molecular Neuropsychiatry Section, Division of Intramural Research, Baltimore, MD 21224, USA.

出版信息

Ann Med Interne (Paris). 2001 Apr;152 Suppl 3:IS57-9.

PMID:11435997
Abstract

3,4-methylenedioxymethamphetamine (MDMA) or ecstasy) is a substituted amphetamine with stimulating and hallucinogenic properties. Administration of MDMA leads to the formation of metabolites responsible for its toxic effects on serotonergic neurons in rats and non-human primates and on dopaminergic neurons in mice. Our findings indicate that overexpression of the human superoxide dismutase gene (Cu/Zn-SOD) abolishes certain effects of MDMA such as the decreased level of dopamine, DOPAC and 5-HT in the striatum, inactivation of certain antioxidant enzymes (CU/ZN-SPD, catalase or glutathione peroxidase) or peroxidation of lipids. These data are in agreement with the implication of free radicals and consequenty of oxidative stress in the mode of action of MDMA.

摘要

3,4-亚甲基二氧甲基苯丙胺(MDMA,即摇头丸)是一种具有刺激和致幻特性的取代苯丙胺。给大鼠和非人类灵长类动物服用MDMA会导致代谢产物的形成,这些代谢产物会对其血清素能神经元产生毒性作用,对小鼠的多巴胺能神经元也有影响。我们的研究结果表明,人类超氧化物歧化酶基因(铜/锌超氧化物歧化酶)的过表达消除了MDMA的某些影响,如纹状体中多巴胺、3,4-二羟基苯乙酸和5-羟色胺水平的降低、某些抗氧化酶(铜/锌超氧化物歧化酶、过氧化氢酶或谷胱甘肽过氧化物酶)的失活或脂质过氧化。这些数据与自由基以及随之而来的氧化应激在MDMA作用模式中的作用相符。

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