Investigation of acute lead poisoning on apoptosis in rat hippocampus in vivo

被引:92
作者
Sharifi, AM
Baniasadi, S
Jorjani, M
Rahimi, F
Bakhshayesh, M
机构
[1] Iran Univ Med Sci, Dept Pharmacol, Tehran, Iran
[2] Iran Univ Med Sci, Cellular & Mol Res Ctr, Tehran, Iran
[3] Shahid Beheshti Univ Med Sci, Dept Pharmacol, Tehran, Iran
[4] Shahid Beheshti Univ Med Sci, Dept Pathol, Taleghani Hosp, Tehran, Iran
关键词
apoptosis; lead poisoning; neurotoxicity; hippocampus; Bax; Bcl-2; protein expression; nuclear fragmentation;
D O I
10.1016/S0304-3940(02)00576-1
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Despite decades of study, the exact mechanism of action of lead, a potent neurotoxic agent, have not been fully elucidated. One of the suggested mechanism of lead neurotoxicity is apoptotic cell death. The present study sought to examine the effect of acute lead poisoning on apoptosis in rat hippocampus. Two to four and 12-14 week old rats were treated for 7 days with 15 mg/kg daily dose of lead acetate intraperitoneally. Control animals received distilled water. In treated groups, the blood lead levels was increased by about 17-19-folds. Histological study of hippocampus revealed apoptotic cells, using light and electron microscopy. In Western blot analysis, the ratio of Bax/Bcl-2 protein expression in hippocampus was significantly increased compared to controls. In conclusion, the lead induced cell death in hippocampus in vivo may partly be due to apoptosis. (C) 2002 Elsevier Science Ireland Ltd. All rights reserved.
引用
收藏
页码:45 / 48
页数:4
相关论文
共 19 条
[1]  
Blaschke AJ, 1998, J COMP NEUROL, V396, P39, DOI 10.1002/(SICI)1096-9861(19980622)396:1<39::AID-CNE4>3.0.CO
[2]  
2-J
[3]   GLUTAMATE NEUROTOXICITY AND DISEASES OF THE NERVOUS-SYSTEM [J].
CHOI, DW .
NEURON, 1988, 1 (08) :623-634
[4]   Lead-induced alterations in retinal cGMP phosphodiesterase trigger calcium overload, mitochondrial dysfunction and rod photoreceptor apoptosis [J].
Fox, DA ;
He, LH ;
Poblenz, AT ;
Medrano, CJ ;
Blocker, YS ;
Srivastava, D .
TOXICOLOGY LETTERS, 1998, 103 :359-361
[5]   SUPPRESSION OF PROGRAMMED NEURONAL DEATH BY SUSTAINED ELEVATION OF CYTOPLASMIC CALCIUM [J].
FRANKLIN, JL ;
JOHNSON, EM .
TRENDS IN NEUROSCIENCES, 1992, 15 (12) :501-508
[6]   Lead and calcium produce rod photoreceptor cell apoptosis by opening the mitochondrial permeability transition pore [J].
He, LH ;
Poblenz, AT ;
Medrano, CJ ;
Fox, DA .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2000, 275 (16) :12175-12184
[7]   BCL-2 IS AN INNER MITOCHONDRIAL-MEMBRANE PROTEIN THAT BLOCKS PROGRAMMED CELL-DEATH [J].
HOCKENBERY, D ;
NUNEZ, G ;
MILLIMAN, C ;
SCHREIBER, RD ;
KORSMEYER, SJ .
NATURE, 1990, 348 (6299) :334-336
[8]   Mechanisms of programmed cell death in the developing brain [J].
Kuan, CY ;
Roth, KA ;
Flavell, RA ;
Rakic, P .
TRENDS IN NEUROSCIENCES, 2000, 23 (07) :291-297
[9]  
Oberto A, 1996, J PHARMACOL EXP THER, V279, P435
[10]   BCL-2 HETERODIMERIZES IN-VIVO WITH A CONSERVED HOMOLOG, BAX, THAT ACCELERATES PROGRAMMED CELL-DEATH [J].
OLTVAI, ZN ;
MILLIMAN, CL ;
KORSMEYER, SJ .
CELL, 1993, 74 (04) :609-619