Reactive oxygen radicals and pathogenesis of neuronal death after cerebral ischemia

被引:279
作者
Sugawara, T
Chan, PH
机构
[1] Stanford Univ, Neurosurg Labs, Sch Med, Dept Neurosurg,Dept Neurol & Neurol Sci, Stanford, CA 94305 USA
[2] Stanford Univ, Neurosci Program, Sch Med, Stanford, CA 94305 USA
关键词
D O I
10.1089/152308603770310266
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
Reactive oxygen species have been implicated in brain injury after cerebral ischemia. These oxidants can damage proteins, lipids, and DNA, and lead to cell injury and necrosis. Oxidants are also initiators in intracellular cell death signaling pathways that may lead to apoptosis. The possible targets of this redox signaling include mitochondria, death membrane receptors, and DNA repair enzymes. Genetic manipulation of intrinsic antioxidants; and the factors in the signaling pathways has provided substantial progress in understanding the mechanisms in cell death signaling pathways and involvement of oxygen radicals in ischemic brain injury. Future studies of these pathways may provide novel therapeutic strategies in clinical stroke.
引用
收藏
页码:597 / 607
页数:11
相关论文
共 111 条
[1]   Glutamate induced cell death: Apoptosis or necrosis? [J].
Ankarcrona, M .
GLUTAMATE SYNAPSE AS A THERAPEUTICAL TARGET: MOLECULAR ORGANIZATION AND PATHOLOGY OF THE GLUTAMATE SYNAPSE, 1998, 116 :265-272
[2]   Interaction of human apurinic endonuclease and DNA polymerase beta in the base excision repair pathway [J].
Bennett, RAO ;
Wilson, DM ;
Wong, D ;
Demple, B .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1997, 94 (14) :7166-7169
[3]   APOPTOSIS AND NECROSIS - 2 DISTINCT EVENTS INDUCED, RESPECTIVELY, BY MILD AND INTENSE INSULTS WITH N-METHYL-D-ASPARTATE OR NITRIC-OXIDE SUPEROXIDE IN CORTICAL CELL-CULTURES [J].
BONFOCO, E ;
KRAINC, D ;
ANKARCRONA, M ;
NICOTERA, P ;
LIPTON, SA .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1995, 92 (16) :7162-7166
[4]   MITOCHONDRIAL GENERATION OF HYDROGEN-PEROXIDE - GENERAL PROPERTIES AND EFFECT OF HYPERBARIC-OXYGEN [J].
BOVERIS, A ;
CHANCE, B .
BIOCHEMICAL JOURNAL, 1973, 134 (03) :707-716
[5]   OXIDATIVE-PHOSPHORYLATION AND PHOTOPHOSPHORYLATION [J].
BOYER, PD ;
CHANCE, B ;
ERNSTER, L ;
MITCHELL, P ;
RACKER, E ;
SLATER, EC .
ANNUAL REVIEW OF BIOCHEMISTRY, 1977, 46 :955-1026
[6]   Altered neuronal and microglial responses to excitotoxic and ischemic brain injury in mice lacking TNF receptors [J].
Bruce, AJ ;
Boling, W ;
Kindy, MS ;
Peschon, J ;
Kraemer, PJ ;
Carpenter, MK ;
Holtsberg, FW ;
Mattson, MP .
NATURE MEDICINE, 1996, 2 (07) :788-794
[7]   Structural and biochemical basis of apoptotic activation by Smac/DIABLO [J].
Chai, JJ ;
Du, CY ;
Wu, JW ;
Kyin, S ;
Wang, XD ;
Shi, YG .
NATURE, 2000, 406 (6798) :855-862
[8]  
CHAN PH, 1993, PROG BRAIN RES, V96, P97
[9]  
CHAN PH, 1994, ANN NY ACAD SCI, V738, P93
[10]   BRAIN INFARCTION IS NOT REDUCED IN SOD-1 TRANSGENIC MICE AFTER A PERMANENT FOCAL CEREBRAL-ISCHEMIA [J].
CHAN, PH ;
KAMII, H ;
YANG, GY ;
GAFNI, J ;
EPSTEIN, CJ ;
CARLSON, E ;
REOLA, L .
NEUROREPORT, 1993, 5 (03) :293-296