The antioxidant defences of brain mitochondria during short-term forebrain ischemia and recirculation in the rat

被引:26
作者
Sims, NR
Williams, VK
Zaidan, E
Powell, JA
机构
[1] Flinders Univ S Australia, Sch Med, Dept Med Biochem, Adelaide, SA 5001, Australia
[2] Flinders Univ S Australia, Sch Med, Ctr Neurosci, Adelaide, SA 5001, Australia
来源
MOLECULAR BRAIN RESEARCH | 1998年 / 60卷 / 02期
基金
英国医学研究理事会;
关键词
ischemia; superoxide dismutase; glutathione peroxidase; glutathione reductase; mitochondrial respiration; oxidative damage;
D O I
10.1016/S0169-328X(98)00172-7
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
This study evaluated changes in the antioxidant defences of mitochondria induced by 30 min of forebrain ischemia and recirculation up to 24 h in rats. Following treatment, mitochondria were isolated from two brain subregions: the dorsolateral striatum, an area in which there is loss of most neurons, and the paramedian cortex in which most neurons are resistant to damage. During ischemia and the first few hours of recirculation, the mitochondrial defences were largely preserved based on measurements of the activities of the enzymes, superoxide dismutase, glutathione peroxidase and glutathione reductase, as well as the response of the mitochondria to a subsequent exposure to H2O2 in vitro. However, some moderate changes were detected, particularly in the mitochondria from the dorsolateral striatum. A decrease of 30% in the activity of superoxide dismutase was seen at the conclusion of the ischemic period and a small increase in susceptibility to changes induced by H2O2 was detected during early recirculation. This latter change preceded and possibly contributed to the development of an impairment of respiratory function detected in mitochondria from the dorsolateral striatum at 3 h of recirculation. At 24 h of recirculation, larger changes were seen in the activities of all three of the enzymes in mitochondria from the dorsolateral striatum but not the paramedian cortex that was associated with progression to advanced neuronal damage in the former subregion. (C) 1998 Elsevier Science B.V. All rights reserved.
引用
收藏
页码:141 / 149
页数:9
相关论文
共 39 条
[1]  
ALMEIDA A, 1995, J NEUROCHEM, V65, P1698
[2]   POSTISCHEMIC INHIBITION OF CEREBRAL-CORTEX PYRUVATE-DEHYDROGENASE [J].
BOGAERT, YE ;
ROSENTHAL, RE ;
FISKUM, G .
FREE RADICAL BIOLOGY AND MEDICINE, 1994, 16 (06) :811-820
[3]   REGIONAL DISTRIBUTION OF GLUTATHIONE-PEROXIDASE IN THE ADULT-RAT BRAIN [J].
BRANNAN, TS ;
MAKER, HS ;
WEISS, C ;
COHEN, G .
JOURNAL OF NEUROCHEMISTRY, 1980, 35 (04) :1013-1014
[4]  
CARLBERG I, 1985, METHOD ENZYMOL, V113, P484
[5]   Role of oxidants in ischemic brain damage [J].
Chan, PH .
STROKE, 1996, 27 (06) :1124-1129
[6]  
CHANCE B, 1956, ADV ENZYMOL REL S BI, V17, P65
[7]  
CHANTAL PJ, 1975, BIOCHEM J, V150, P31
[8]   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
[9]  
Dean RT, 1997, BIOCHEM J, V324, P1
[10]   The importance of sodium pyruvate in assessing damage produced by hydrogen peroxide [J].
Giandomenico, AR ;
Cerniglia, GE ;
Biaglow, JE ;
Stevens, CW ;
Koch, CJ .
FREE RADICAL BIOLOGY AND MEDICINE, 1997, 23 (03) :426-434