Protective effects of S-nitrosoglutathione against neurotoxicity of 3-nitropropionic acid in rat

被引：31

作者：

Ju, TC ^{[1
]}

Yang, YT ^{[1
]}

Yang, DI ^{[1
]}

机构：

[1] Tzu Chi Univ, Inst Neurosci, Hualien 970, Taiwan

来源：

NEUROSCIENCE LETTERS | 2004年 / 362卷 / 03期

关键词：

mitochondrial toxin; nitric oxide; oxidative stress; S-nitrosothiol;

D O I：

10.1016/j.neulet.2004.03.028

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

Mitochondrial dysfunction and oxidative stress are often linked to various neurodegenerative disorders including ischemic stroke and Huntington's disease (HD). S-Nitrosoglutathione (GSNO) is an endogenous nitric oxide carrier recently identified as a potent antioxidant capable of neutralizing oxidative stress. In the present study, we explore the neuroprotective effects of GSNO against metabolic insults induced by 3-nitropropionic acid (3-NP), a mitochondrial complex II inhibitor commonly used as a pharmacological model for HID, in primary culture of fetal rat cortical and striatal neurons. Application of GSNO (1-5 muM) substantially reduced neuronal loss caused by 3-NP (1-5 mM) exposure based on MTT reduction, lactate dehydrogenase (LDH) release, and Hoechst staining assays. The protective effect of GSNO appeared to be more potent than N-acetyl-L-cysteine (NAC), a glutathione precursor, at the same concentrations. These results suggest that manipulation of GSNO metabolism may exert protective effects against mitochondrial dysfunction often observed in neurodegenerative disorders. (C) 2004 Elsevier Ireland Ltd. All rights reserved.

引用

页码：226 / 231

页数：6

共 30 条

[1] Neocuproine, a selective Cu(I) chelator, and the relaxation of rat vascular smooth muscle by S-nitrosothiols [J].