Oxidative and antioxidative potential of brain microglial cells

被引:209
作者
Dringen, R
机构
[1] Univ Bremen, Ctr Biomol Interact Bremen, Fac Biol Chem 2, D-28334 Bremen, Germany
[2] Monash Univ, Dept Psychol, Clayton, Vic 3168, Australia
关键词
D O I
10.1089/ars.2005.7.1223
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Microglial cells are the resident immune cells of the central nervous system. These cells defend the central nervous system against invading microorganisms and clear the debris from damaged cells. Upon activation, microglial cells produce a large number of neuroactive substances that include cytokines, proteases, and prostanoids. In addition, activated microglial cells release radicals, such as superoxide and nitric oxide, that are products of the enzymes NADPH oxidase and inducible nitric oxide synthase, respectively. Microglia-derived radicals, as well as their reactive reaction products hydrogen peroxide and peroxynitrite, have the potential to harm cells and have been implicated in contributing to oxidative damage and neuronal cell death in neurological diseases. For self-protection against oxidative damage, microglial cells are equiped with efficient antioxidative defense mechanisms. These cells contain glutathione in high concentrations, substantial activities of the antioxidative enzymes superoxide dismutase, catalase, glutathione peroxidase, and glutathione reductase, as well as NADPH-regenerating enzymes. Their good antioxidative potential protects microglial cells against oxidative damage that could impair important functions of these cells in defense and repair of the brain.
引用
收藏
页码:1223 / 1233
页数:11
相关论文
共 132 条
[51]   Microglia as a source and target of cytokines [J].
Hanisch, UK .
GLIA, 2002, 40 (02) :140-155
[52]   Induction of argininosuccinate synthetase in rat brain glial cells after striatal microinjection of immunostimulants [J].
Heneka, MT ;
Schmidlin, A ;
Wiesinger, H .
JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM, 1999, 19 (08) :898-907
[53]   Neuronal and glial coexpression of argininosuccinate synthetase and inducible nitric oxide synthase in Alzheimer disease [J].
Heneka, MT ;
Wiesinger, H ;
Dumitrescu-Ozimek, L ;
Riederer, P ;
Feinstein, DL ;
Klockgether, T .
JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY, 2001, 60 (09) :906-916
[54]  
Heppner FL, 1998, GLIA, V22, P180, DOI 10.1002/(SICI)1098-1136(199802)22:2<180::AID-GLIA9>3.0.CO
[55]  
2-B
[56]   Encephalopathy in megacystis-microcolon-intestinal hypoperistalsis syndrome patients on long-term total parenteral nutrition possibly due to selenium deficiency [J].
Hirato, J ;
Nakazato, Y ;
Koyama, H ;
Yamada, A ;
Suzuki, N ;
Kuroiwa, M ;
Takahashi, A ;
Matsuyama, S ;
Asayama, K .
ACTA NEUROPATHOLOGICA, 2003, 106 (03) :234-242
[57]   Oligodendroglial cells in culture effectively dispose of exogenous hydrogen peroxide: comparison with cultured neurones, astroglial and microglial cells [J].
Hirrlinger, J ;
Resch, A ;
Gutterer, JM ;
Dringen, R .
JOURNAL OF NEUROCHEMISTRY, 2002, 82 (03) :635-644
[58]   Microglial cells in culture express a prominent glutathione system for the defense against reactive oxygen species [J].
Hirrlinger, J ;
Gutterer, JM ;
Kussmaul, L ;
Hamprecht, B ;
Dringen, R .
DEVELOPMENTAL NEUROSCIENCE, 2000, 22 (5-6) :384-392
[59]   Glial cell type-specific responses to menadione-induced oxidative stress [J].
Hollensworth, SB ;
Shen, CC ;
Sim, JE ;
Spitz, DR ;
Wilson, GL ;
LeDoux, SP .
FREE RADICAL BIOLOGY AND MEDICINE, 2000, 28 (08) :1161-1174
[60]   MEASUREMENT OF STRIATAL H2O2 BY MICRODIALYSIS FOLLOWING GLOBAL FOREBRAIN ISCHEMIA AND REPERFUSION IN THE RAT - CORRELATION WITH THE CYTOTOXIC POTENTIAL OF H2O2 IN-VITRO [J].
HYSLOP, PA ;
ZHANG, ZY ;
PEARSON, DV ;
PHEBUS, LA .
BRAIN RESEARCH, 1995, 671 (02) :181-186