Antioxidants for CNS ischaemia and trauma

被引:7
作者
Ringel, F [1 ]
Schmid-Elsaesser, R [1 ]
机构
[1] Univ Munich, Klinikum Grosshadern, Dept Neurosurg, D-81377 Munich, Germany
关键词
antioxidants; cerebral ischaemia; reactive nitrogen species; reactive oxygen species; spinal cord injuries; spinal cord ischaemia; traumatic brain injuries;
D O I
10.1517/13543776.11.6.987
中图分类号
R914 [药物化学];
学科分类号
100701 ;
摘要
CNS ischaemia and trauma are leading causes of death or severe disabilities worldwide. However, so far, few treatment options are available and current treatment modalities exert only moderate beneficial effects on the outcome of patients. A possible target for the invention of new treatment options is the tissue damage mediated by oxidative stress through reactive oxygen species (ROS) or reactive nitrogen species (RNS). This review outlines the processes leading to the formation of oxidative stress and discusses recent patent applications for antioxidative compounds.
引用
收藏
页码:987 / 997
页数:11
相关论文
共 74 条
[1]   Glutamate neurotoxicity in rat cerebellar granule cells: A major role for xanthine oxidase in oxygen radical formation [J].
Atlante, A ;
Gagliardi, S ;
Minervini, GM ;
Ciotti, MT ;
Marra, E ;
Calissano, P .
JOURNAL OF NEUROCHEMISTRY, 1997, 68 (05) :2038-2045
[2]   Cytochrome c is released from mitochondria in a reactive oxygen species (ROS)-dependent fashion and can operate as a ROS scavenger and as a respiratory substrate in cerebellar neurons undergoing excitotoxic death [J].
Atlante, A ;
Calissano, P ;
Bobba, A ;
Azzariti, A ;
Marra, E ;
Passarella, S .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2000, 275 (47) :37159-37166
[3]  
Bogousslavsky J, 1998, CEREBROVASC DIS, V8, P59
[4]  
Bolanos JP, 1997, J NEUROCHEM, V68, P2227
[5]   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
[6]   MITOCHONDRIAL GENERATION OF HYDROGEN-PEROXIDE - GENERAL PROPERTIES AND EFFECT OF HYPERBARIC-OXYGEN [J].
BOVERIS, A ;
CHANCE, B .
BIOCHEMICAL JOURNAL, 1973, 134 (03) :707-716
[7]   Delayed treatment with AM-36, a novel neuroprotective agent, reduces neuronal damage after endothelin-1-induced middle cerebral artery occlusion in conscious rats [J].
Callaway, JK ;
Knight, MJ ;
Watkins, DJ ;
Beart, PM ;
Jarrott, B .
STROKE, 1999, 30 (12) :2704-2712
[8]   PROTECTION AGAINST OXIDATIVE DAMAGE TO CNS BY ALPHA-PHENYL-TERT-BUTYL NITRONE (PBN) AND OTHER SPIN-TRAPPING AGENTS - A NOVEL SERIES OF NONLIPID FREE-RADICAL SCAVENGERS [J].
CARNEY, JM ;
FLOYD, RA .
JOURNAL OF MOLECULAR NEUROSCIENCE, 1991, 3 (01) :47-57
[9]   Overexpression of SOD1 in transgenic rats protects vulnerable neurons against ischemic damage after global cerebral ischemia and reperfusion [J].
Chan, PH ;
Kawase, M ;
Murakami, K ;
Chen, SF ;
Li, YB ;
Calagui, B ;
Reola, L ;
Carlson, E ;
Epstein, CJ .
JOURNAL OF NEUROSCIENCE, 1998, 18 (20) :8292-8299
[10]   THE ANTIOXIDANT LY231617 REDUCES GLOBAL ISCHEMIC NEURONAL INJURY IN RATS [J].
CLEMENS, JA ;
SAUNDERS, RD ;
HO, PP ;
PHEBUS, LA ;
PANETTA, JA .
STROKE, 1993, 24 (05) :716-722