Postischemic accumulation of lipid peroxidation products in the rat brain: immunohistochemical detection of 4-hydroxy-2-nonenal modified proteins

被引:43
作者
Yoshino, H
Hattori, N
Urabe, T
Uchida, K
Tanaka, M
Mizuno, Y
机构
[1] JUNTENDO UNIV,SCH MED,DEPT NEUROL,BUNKYO KU,TOKYO 113,JAPAN
[2] NAGOYA UNIV,SCH AGR,LAB FOOD & BIODYNAM,NAGOYA,AICHI 464,JAPAN
[3] GIFU INT INST BIOTECHNOL,DEPT GENE THERAPY,GIFU,JAPAN
关键词
middle cerebral artery occlusion and reperfusion; 4-hydroxy-2-nonenal; lipid peroxidation; OX-42; microglia; immunohistochemistry; neuronal death;
D O I
10.1016/S0006-8993(97)00616-1
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
We report an immunohistochemical study on the distribution and alterations of 4-hdrooxy-2-nonenal (HNE)-modified proteins, an indicator of lipid peroxidation, in the rat brain after 3 h of middle cerebral artery (MCA) occlusion followed by reperfusion. HNE immunoreactivity was not observed in intact neurons, but it appeared in some shrunken neurons within the infarcted zone at 3 h after reperfusion. The number of HNE-positive neurons increased with the spread of the infarcted area. The pyramidal neurons in the third layer of the frontoparietal cortex were HNE-positive and the intensity of their HNE immunoreactivity was highest at 24 h after reperfusion. At 48 h, HNE-positive neurons were observed in the medial part of the striatum, the lateral side of the frontoparietal cortex, and at the boundary between the infarcted and noninfarcted zones. In addition, strong HNE immunoreactivity was seen in microglia (identified by OX-42 immunostaining). This method seems to be useful to follow the progress of lipid peroxidation at the cellular level after ischemic injury. (C) 1997 Elsevier Science B.V.
引用
收藏
页码:81 / 86
页数:6
相关论文
共 38 条
[1]   4-HYDROXYRMONENAL, A NOVEL INDICATOR OF LIPID-PEROXIDATION FOR REPERFUSION INJURY OF THE MYOCARDIUM [J].
BLASIG, IE ;
GRUNE, T ;
SCHONHEIT, K ;
ROHDE, E ;
JAKSTADT, M ;
HASELOFF, RF ;
SIEMS, WG .
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY, 1995, 269 (01) :H14-H22
[2]   MICROGLIAL-PRODUCED NITRIC-OXIDE AND REACTIVE NITROGEN-OXIDES MEDIATE NEURONAL CELL-DEATH [J].
BOJE, KM ;
ARORA, PK .
BRAIN RESEARCH, 1992, 587 (02) :250-256
[3]   INCREASED LIPID-PEROXIDATION IN VULNERABLE BRAIN-REGIONS AFTER TRANSIENT FOREBRAIN ISCHEMIA IN RATS [J].
BROMONT, C ;
MARIE, C ;
BRALET, J .
STROKE, 1989, 20 (07) :918-924
[4]   Role of oxidants in ischemic brain damage [J].
Chan, PH .
STROKE, 1996, 27 (06) :1124-1129
[5]  
CHAO CC, 1992, J IMMUNOL, V149, P2736
[6]   BCL-2 IS EXPRESSED IN NEURONS THAT SURVIVE FOCAL ISCHEMIA IN THE RAT [J].
CHEN, J ;
GRAHAM, SH ;
CHAN, PH ;
LAN, JQ ;
ZHOU, RL ;
SIMON, RP .
NEUROREPORT, 1995, 6 (02) :394-398
[7]   ALTERATIONS IN MITOCHONDRIAL-MEMBRANE FLUIDITY BY LIPID-PEROXIDATION PRODUCTS [J].
CHEN, JJ ;
YU, BP .
FREE RADICAL BIOLOGY AND MEDICINE, 1994, 17 (05) :411-418
[8]   PRODUCTION OF SUPEROXIDE ANIONS BY A CNS MACROPHAGE, THE MICROGLIA [J].
COLTON, CA ;
GILBERT, DL .
FEBS LETTERS, 1987, 223 (02) :284-288
[9]   CHEMISTRY AND BIOCHEMISTRY OF 4-HYDROXYNONENAL, MALONALDEHYDE AND RELATED ALDEHYDES [J].
ESTERBAUER, H ;
SCHAUR, RJ ;
ZOLLNER, H .
FREE RADICAL BIOLOGY AND MEDICINE, 1991, 11 (01) :81-128
[10]   IMMUNOCYTOCHEMICAL STUDY OF AN EARLY MICROGLIAL ACTIVATION IN ISCHEMIA [J].
GEHRMANN, J ;
BONNEKOH, P ;
MIYAZAWA, T ;
HOSSMANN, KA ;
KREUTZBERG, GW .
JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM, 1992, 12 (02) :257-269