Selenium, an antioxidant, protects against methamphetamine-induced dopaminergic neurotoxicity

被引：67

作者：

Imam, SZ

Newport, GD

Islam, F

Slikker, W

Ali, SF

机构：

[1] US FDA, Natl Ctr Toxicol Res, Div Neurotoxicol, Neurochem Lab, Jefferson, AR 72079 USA

[2] Hamdard Univ, Dept Med Elementol & Toxicol, Neurotoxicol Lab, New Delhi, India

[3] Univ Arkansas Med Sci, Dept Neurol & Biochem & Mol Biol, Little Rock, AR 72205 USA

来源：

BRAIN RESEARCH | 1999年 / 818卷 / 02期

关键词：

methamphetamine; neurotoxicity; selenium; dopamine; caudate nucleus; oxidative stress;

D O I：

10.1016/S0006-8993(98)01311-0

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

Dopaminergic changes were studied in the caudate nucleus of adult female mice after pre- and post-treatment with an antioxidant, selenium, 72 h after the multiple injections of methamphetamine (METH, 4 x 10 mg/kg, i.p. at 2-h interval) or an equivalent volume of saline. Selenium treatment prevented the depletion of dopamine (DA) and its metabolites 3,4-dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA) in caudate nucleus resulting from the METH treatment. These data suggest that METH-induced neurotoxicity is mediated by free radical and selenium plays a protective role against METH-induced dopaminergic neurotoxicity. (C) 1999 Elsevier Science B.V. All rights reserved.

引用

页码：575 / 578

页数：4

共 31 条

[1] LOW ENVIRONMENTAL TEMPERATURES OR PHARMACOLOGICAL AGENTS THAT PRODUCE HYPOTHERMIA DECREASE METHAMPHETAMINE NEUROTOXICITY IN MICE [J].