Nitric-oxide-induced inhibition of mitochondrial complexes following aglycaemic hypoxia in neonatal cortical rat brain slices

被引:13
作者
Brooks, KJ
Hargreaves, IP
Bates, TE
机构
[1] UCL Hosp, Sch Med, Rayne Inst, Dept Paediat, London, England
[2] Natl Hosp Neurol & Neurosurg, Dept Clin Biochem, London, England
[3] UCL, Inst Neurol, Dept Neurochem, London WC1E 6BT, England
关键词
brain; ischaemia; neonate; mitochondria; complexes;
D O I
10.1159/000017461
中图分类号
Q [生物科学];
学科分类号
07 ; 0710 ; 09 ;
摘要
The effect of aglycaemic hypoxia (AH) on the activity of the mitochondrial respiratory chain complexes was measured in superfused neonatal cortical brain slices. After 30 min AH, there were no significant changes in the activities of complex 1, II-III and IV or citrate synthase compared to controls. Following 30 min AH and a 30-min reperfusion period (with oxygen and glucose), the activities of complex II-III and complex IV were significantly reduced (by 25 and 17%, respectively). These reductions in enzyme activity were not abrogated by removing external calcium prior to and throughout AH, but could be reversed by the presence of the nitric oxide (NO) synthase inhibitor No-nitro-L-arginine during these periods. These data suggest that NO or an NO-derived species is involved in the decreases in mitochondrial enzyme activities observed after AH Copyright (C) 2000 S. Karger AG,Basel.
引用
收藏
页码:359 / 365
页数:7
相关论文
共 43 条
[1]  
ALLEN KL, 1995, J NEUROCHEM, V64, P2222
[2]  
ALMEIDA A, 1995, J NEUROCHEM, V65, P1698
[3]   P-31 NMR-STUDIES ON SUPERFUSED CEREBRAL TISSUES [J].
BACHELARD, HS ;
COX, DWG ;
FEENEY, J ;
MORRIS, PG .
BIOCHEMICAL SOCIETY TRANSACTIONS, 1985, 13 (05) :835-839
[4]   APPARENT HYDROXYL RADICAL PRODUCTION BY PEROXYNITRITE - IMPLICATIONS FOR ENDOTHELIAL INJURY FROM NITRIC-OXIDE AND SUPEROXIDE [J].
BECKMAN, JS ;
BECKMAN, TW ;
CHEN, J ;
MARSHALL, PA ;
FREEMAN, BA .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1990, 87 (04) :1620-1624
[5]   Increased nitric oxide synthesis is not involved in delayed cerebral energy failure following focal hypoxic-ischemic injury to the developing brain [J].
Blumberg, RM ;
Taylor, DL ;
Yue, X ;
Aguan, K ;
Mckenzie, J ;
Cady, EB ;
Weiner, CP ;
Mehmet, H ;
Edwards, AD .
PEDIATRIC RESEARCH, 1999, 46 (02) :224-231
[6]   Relation between delayed impairment of cerebral energy metabolism and infarction following transient focal hypoxia-ischaemia in the developing brain [J].
Blumberg, RM ;
Cady, EB ;
Wigglesworth, JS ;
McKenzie, JE ;
Edwards, AD .
EXPERIMENTAL BRAIN RESEARCH, 1997, 113 (01) :130-137
[7]  
BOLANOS JP, 1994, J NEUROCHEM, V63, P910
[8]  
BOLANOS JP, 1995, J NEUROCHEM, V64, P1965
[9]  
Brooks KJ, 1998, J NEUROCHEM, V70, P1986
[10]   CALCIUM-MEDIATED DAMAGE FOLLOWING HYPOXIA IN CEREBRAL-CORTEX EX-VIVO STUDIED BY NMR-SPECTROSCOPY - EVIDENCE FOR DIRECT INVOLVEMENT OF VOLTAGE-GATED CA2+-CHANNELS [J].
BROOKS, KJ ;
KAUPPINEN, RA .
NEUROCHEMISTRY INTERNATIONAL, 1993, 23 (05) :441-450