Lipid peroxidation in hippocampus early and late after status epilepticus induced by pilocarpine or kainic acid in Wistar rats

被引：149

作者：

Dal-Pizzol, F

Klamt, F

Vianna, MMR

Schröder, N

Quevedo, J

Benfato, MS

Moreira, JCF

Walz, R

机构：

[1] Univ Fed Rio Grande Sul, Inst Ciencias Basicas Saude, Dept Bioquim, Lab Estresse Oxidat, Porto Alegre, RS, Brazil

[2] Univ Fed Rio Grande Sul, Inst Ciencias Basicas Saude, Dept Bioquim, Ctr Memoria, Porto Alegre, RS, Brazil

[3] Univ Fed Rio Grande Sul, Inst Biociencias, Dept Biofis, Porto Alegre, RS, Brazil

[4] Hosp Reg Sao Jose, Serv Neurol, Sao Jose, SC, Brazil

来源：

NEUROSCIENCE LETTERS | 2000年 / 291卷 / 03期

关键词：

oxidative stress; status epilepticus; kainic acid; pilocarpine; epilepsy; lipid peroxidation; thiobarbituric acid reactive substances;

D O I：

10.1016/S0304-3940(00)01409-9

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

Oxidative stress has been implicated in a variety of acute and chronic neurologic conditions, including epilepsy. Both the kainic acid and pilocarpine are useful models of temporal lobe epilepsy in rodents. As an index of lipid peroxidation the level thiobarbituric acid reactive substances (TBARS) was measured after the status epileticus induced by pilocarpine or kainic acid. In hippocampus there was a slight enhancement in the TBARS levels measured 12-14 h after the end of status epileticus induced by pilocarpine and kainic acid. The TBARS levels in pilocarpine treated animals was significantly decreased late after status epileticus and in kainic acid model the TBARS returned to basal levels. These results indicating a putative role of reactive oxygen species in kainic acid and pilocarpine induced epilepsy. (C) 2000 Elsevier Science Ireland Ltd. All rights reserved.

引用

页码：179 / 182

页数：4

共 19 条

[1]

[Anonymous], FREE RADICALS BIOL M

[2] LIMBIC SEIZURE AND BRAIN-DAMAGE PRODUCED BY KAINIC ACID - MECHANISMS AND RELEVANCE TO HUMAN TEMPORAL-LOBE EPILEPSY [J].

BENARI, Y .

NEUROSCIENCE, 1985, 14 (02) :375-403

[3] Changes in synaptosomal ectonucleotidase activities in two rat models of temporal lobe epilepsy [J].

Bonan, CD ;

Walz, R ;

Pereira, GS ;

Worm, PV ;

Battastini, AMO ;

Cavalheiro, EA ;

Izquierdo, I ;

Sarkis, JJF .

EPILEPSY RESEARCH, 2000, 39 (03) :229-238

[4] OXIDATIVE STRESS-INDUCED BY GLUTAMATE RECEPTOR AGONISTS [J].

BONDY, SC ;

LEE, DK .

BRAIN RESEARCH, 1993, 610 (02) :229-233

[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] OXYGEN-FREE RADICALS IN RAT LIMBIC STRUCTURES AFTER KAINATE-INDUCED SEIZURES [J].

BRUCE, AJ ;

BAUDRY, M .

FREE RADICAL BIOLOGY AND MEDICINE, 1995, 18 (06) :993-1002

[7] LONG-TERM EFFECTS OF PILOCARPINE IN RATS - STRUCTURAL DAMAGE OF THE BRAIN TRIGGERS KINDLING AND SPONTANEOUS RECURRENT SEIZURES [J].

CAVALHEIRO, EA ;

LEITE, JP ;

BORTOLOTTO, ZA ;

TURSKI, WA ;

IKONOMIDOU, C ;

TURSKI, L .

EPILEPSIA, 1991, 32 (06) :778-782

[8] ELECTROPHYSIOLOGY OF DENTATE GRANULE CELLS AFTER KAINATE-INDUCED SYNAPTIC REORGANIZATION OF THE MOSSY FIBERS [J].

CRONIN, J ;

OBENAUS, A ;

HOUSER, CR ;

DUDEK, FE .

BRAIN RESEARCH, 1992, 573 (02) :305-310

[9]

DRAPER HH, 1990, METHOD ENZYMOL, V186, P421

[10] LOCAL CEREBRAL METABOLISM DURING PARTIAL SEIZURES [J].

ENGEL, J ;

KUHL, DE ;

PHELPS, ME ;

RAUSCH, R ;

NUWER, M .

NEUROLOGY, 1983, 33 (04) :400-413

← 1 2 →