Ethanol and oxidative mechanisms in the brain

被引:92
作者
Sun, AY [1 ]
Sun, GY
机构
[1] Univ Missouri, Dept Pharmacol, Columbia, MO 65212 USA
[2] Univ Missouri, Dept Biochem, Columbia, MO 65212 USA
关键词
ethanol; oxidative neuronal damage; resveratrol; polyphenols;
D O I
10.1007/BF02255969
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
There is strong evidence showing that chronic and excessive ethanol consumption may enhance oxidative damage to neurons and result in cell death. Although not yet well understood, ethanol may enhance ROS production in brain through a number of pathways including increased generation of hydroxyethyl radicals, induction of CYP2E1, alteration of the cytokine signaling pathways for induction of iNOS and sPLA(2), and production of prostanoids through the PLA(2)/COX pathways. Since many neurodegenerative diseases are also associated with oxidative and inflammatory mechanisms in the brain, it would be important to find out whether chronic and excessive ethanol consumption may exacerbate the progression of these diseases. There is evidence that the polyphenolic antioxidants, especially those extracted from grape skin and seed, may protect the brain from neuronal damage due to chronic ethanol administration. Among the polyphenols from grapes, resveratrol seems to have unique antioxidant properties. The possible use of this compound as a therapeutic agent to ameliorate neurodegenerative processes should be further explored. Copyright (C) 2001 National Science Council. ROC and S. Karger AG. Basel.
引用
收藏
页码:37 / 43
页数:7
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