Effect of Chronic Lead Exposure on Pro-Apoptotic Bax and Anti-Apoptotic Bcl-2 Protein Expression in Rat Hippocampus In Vivo |
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Authors: | Ali M Sharifi Seyed Hadi Mousavi Masoumeh Jorjani |
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Institution: | (1) Department of Pharmacology, School of Medicine, Iran University of Medical Sciences, Tehran, Iran;(2) Razi Institute for Drug Research, Iran University of Medical Sciences, Tehran, Iran;(3) Endocrinology and Metabolism Research Center (EMRC), Shariati hospital, Tehran, Iran;(4) Department of Pharmacology & Medical Toxicology Research Center, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran;(5) Department of Pharmacology, Medical School, Shahid Beheshti University of Medical Sciences, Tehran, Iran |
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Abstract: | 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. |
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