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
[61]   Nitric oxide as a signaling molecule in the vascular system: An overview [J].
Ignarro, LJ ;
Cirino, G ;
Casini, A ;
Napoli, C .
JOURNAL OF CARDIOVASCULAR PHARMACOLOGY, 1999, 34 (06) :879-886
[62]   Involvement of inducible nitric oxide synthase in inflammation-induced dopaminergic neurodegeneration [J].
Iravani, MM ;
Kashefi, K ;
Mander, P ;
Rose, S ;
Jenner, P .
NEUROSCIENCE, 2002, 110 (01) :49-58
[63]   Oxidative stress in Parkinson's disease [J].
Jenner, P .
ANNALS OF NEUROLOGY, 2003, 53 :S26-S36
[64]   Reversal of thiamine deficiency-induced neurodegeneration [J].
Ke, ZJ ;
DeGiorgio, LA ;
Volpe, BT ;
Gibson, GE .
JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY, 2003, 62 (02) :195-207
[65]   Microglia and chemokines in infectious diseases of the nervous system: Views and reviews [J].
Kielian, T .
FRONTIERS IN BIOSCIENCE-LANDMARK, 2004, 9 :732-750
[66]   Pathways of neuron-astrocyte interactions and their possible role in neuroprotection [J].
Kirchhoff, F ;
Dringen, R ;
Giaume, C .
EUROPEAN ARCHIVES OF PSYCHIATRY AND CLINICAL NEUROSCIENCE, 2001, 251 (04) :159-169
[67]   Manganese superoxide dismutase overexpression attenuates MPTP toxicity [J].
Klivenyi, P ;
St Clair, D ;
Wermer, M ;
Yen, HC ;
Oberley, T ;
Yang, LC ;
Beal, MF .
NEUROBIOLOGY OF DISEASE, 1998, 5 (04) :253-258
[68]   Long-term induction of haem oxygenase-1 (HSP-32) in astrocytes and microglia following transient focal brain ischaemia in the rat [J].
Koistinaho, J ;
Miettinen, S ;
Keinanen, R ;
Vartiainen, N ;
Roivainen, R ;
Laitinen, JT .
EUROPEAN JOURNAL OF NEUROSCIENCE, 1996, 8 (11) :2265-2272
[69]  
Koutsilieri E., 2002, J NEUROL, V249, P111, DOI DOI 10.1007/S00415-002-1201-7
[70]   Hydrogen peroxide and ADP-ribose induce TRPM2-mediated calcium influx and cation currents in microglia [J].
Kraft, R ;
Grimm, C ;
Grosse, K ;
Hoffmann, A ;
Sauerbruch, S ;
Kettenmann, H ;
Schultz, G ;
Harteneck, C .
AMERICAN JOURNAL OF PHYSIOLOGY-CELL PHYSIOLOGY, 2004, 286 (01) :C129-C137