Effect of Chronic Lead Exposure on Pro-Apoptotic Bax and Anti-Apoptotic Bcl-2 Protein Expression in Rat Hippocampus In Vivo

被引:48
|
作者
Sharifi, Ali M. [1 ,2 ,3 ]
Mousavi, Seyed Hadi [2 ,4 ,5 ]
Jorjani, Masoumeh [6 ]
机构
[1] Iran Univ Med Sci, Sch Med, Dept Pharmacol, Tehran, Iran
[2] Iran Univ Med Sci, Razi Inst Drug Res, Tehran, Iran
[3] Shariati Hosp, EMRC, Tehran, Iran
[4] Mashhad Univ Med Sci, Sch Med, Dept Pharmacol, Mashhad, Iran
[5] Mashhad Univ Med Sci, Sch Med, Med Toxicol Res Ctr, Mashhad, Iran
[6] Shahid Beheshti Univ Med Sci, Sch Med, Dept Pharmacol, Tehran, Iran
关键词
Apoptosis; Lead neurotoxicity; Hippocampus; Bax; Bcl-2; Protein expression; SEQUENCE SIMILARITY; FAMILY PROTEINS; DEATH; NEUROTOXICITY; GENE; CHILDREN; NEURONS;
D O I
10.1007/s10571-010-9504-1
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Despite reduction in environmental lead, chronic lead exposure still possess a public health hazard, particularly in children, with devastating effects on developing CNS. To investigate the mechanism of this neurotoxicity, young and adult rats were used to study whether exposure to 500 ppm concentrations of lead could induce apoptosis in hippocampus. 2-4 and 12-14-week-old rats received lead acetate in concentration of 500 ppm for 40 days. Control animals received deionized distilled water. In lead-treated groups, the blood lead levels were increased by 3-4 folds. Light and electron microscopical study of hippocampus revealed increased apoptotic cells. Western blot analysis of Bax and Bcl-2 (pro- and anti-apoptotic gene products, respectively) indicated higher expression of Bax protein and no significant change in bcl-2 expression and accordingly increased the Bax/Bcl-2 ratio compared to control group, confirming the histological study. In conclusion, these data suggest that neurotoxicity of chronic lead exposure in hippocampus in vivo may partly be due to facilitation of apoptosis.
引用
收藏
页码:769 / 774
页数:6
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