Document Detail


Lead stimulates ERK1/2 and p38MAPK phosphorylation in the hippocampus of immature rats.
MedLine Citation:
PMID:  14725969     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Lead (Pb(2+)) is widely recognized as a neurotoxicant whose mechanisms of action are not completely established. We have previously demonstrated that Pb(2+) can activate the p38(MAPK) pathway and increase the phosphorylation of Hsp27 in bovine adrenal chromaffin cells and human SH SY5Y cells over a short incubation period (1 h). In the present work we analyzed the effects of Pb(2+) administered in vivo on the level and the phosphorylation state of ERK1/2 and p38(MAPK) in the hippocampus of immature rats. Rats were treated with lead acetate (2, 8 or 12 mg/kg, i.p.) or saline (control) over the 8th to 12th postnatal days, and hippocampal slices were prepared on the 14th day. The Pb(2+) level in the lead-treated animals increased 2.5-6-fold in the blood (3.0-6.0 microg/dl) and 2.0-3.0-fold in the forebrain (78-103 ng/g wet weight), compared to control (saline). The phosphorylation of both ERK1/2 and p38(MAPK) was significantly increased by prior exposure to Pb(2+) in vivo. In in vitro experiments, hippocampal slices from 14-day-old rats were exposed to Pb(2+) (1-10 microM) for 1 and 3 h. There were no changes in the phosphorylation state of ERK and p38(MAPK) for 1-h incubation, whereas a significant increase of ERK1/2 and p38(MAPK) phosphorylation by Pb(2+) (5 microM) was observed for the 3-h incubation. Cell viability measured using MTT was not modified in any of the conditions tested. These results indicate that the phosphorylation of hippocampal ERK1/2 and p38(MAPK) is stimulated by lead in a period of rapid brain development, an effect that may underlie, at least in part, the neurotoxicty elicited by this metal.
Authors:
Fabiano M Cordova; Ana Lúcia S Rodrigues; Maria B O Giacomelli; Camila S Oliveira; Thaís Posser; Peter R Dunkley; Rodrigo B Leal
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Publication Detail:
Type:  Comparative Study; In Vitro; Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Brain research     Volume:  998     ISSN:  0006-8993     ISO Abbreviation:  Brain Res.     Publication Date:  2004 Feb 
Date Detail:
Created Date:  2004-01-16     Completed Date:  2004-03-22     Revised Date:  2009-11-19    
Medline Journal Info:
Nlm Unique ID:  0045503     Medline TA:  Brain Res     Country:  Netherlands    
Other Details:
Languages:  eng     Pagination:  65-72     Citation Subset:  IM    
Affiliation:
Departamento de Bioquímica, Centro de Ciências Biológicas, Universidade Federal de Santa Catarina, SC, 88040-900, Florianópolis, Brazil.
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MeSH Terms
Descriptor/Qualifier:
Analysis of Variance
Animals
Animals, Newborn
Blotting, Western
Cell Survival / drug effects
Female
Hippocampus / drug effects*,  metabolism
Lead / metabolism,  toxicity*
Male
Maximum Tolerated Dose
Mitogen-Activated Protein Kinase 1 / metabolism*
Mitogen-Activated Protein Kinase 3
Mitogen-Activated Protein Kinases / metabolism*
Phosphorylation / drug effects
Prosencephalon / drug effects,  metabolism
Rats
Rats, Wistar
Time Factors
p38 Mitogen-Activated Protein Kinases
Chemical
Reg. No./Substance:
7439-92-1/Lead; EC 2.7.11.24/Mitogen-Activated Protein Kinase 1; EC 2.7.11.24/Mitogen-Activated Protein Kinase 3; EC 2.7.11.24/Mitogen-Activated Protein Kinases; EC 2.7.11.24/p38 Mitogen-Activated Protein Kinases

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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