Document Detail


Effects of subchronic perfluorooctane sulfonate exposure of rats on calcium-dependent signaling molecules in the brain tissue.
MedLine Citation:
PMID:  20127074     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Perfluorooctane sulfonate (PFOS) is a persistent and bio-accumulative pollutant ubiquitous in wildlife and humans, which receives many concerns on the fate, transport, distribution, and toxicity. Studies have shown that PFOS-induced neurotoxicity in experimental animals; however, little is known about the potential mechanism of PFOS exposure on the central nervous system (CNS). Ca(2+)/calmodulin-dependent protein kinase IIalpha (CaMKIIalpha), cAMP-response element binding protein (CREB), c-fos, and c-jun, which are important down-stream molecules of calcium signaling in describing neuron cells structure and function in the CNS, were examined in the paper with the purpose to evaluate the effect of PFOS exposure on brain and approach the molecular mechanisms involved in the neurotoxicity induced by PFOS. Adult male Sprague-Dawley rats were administered with PFOS at dosages of 1.7, 5.0, and 15.0 mg/L in drinking water for 91 consecutive days. LC/MS was used for PFOS analysis in brain tissues, and western blot was employed to determine the expression of CaMKIIalpha and pCREB in the isolated cortex and hippocampus. The expression of c-fos and c-jun was detected by real-time reverse transcription polymerase chain reaction. The results showed that the expression of CaMKIIalpha and pCREB exhibits a significant increase in cortex and hippocampus after treatment with PFOS, compared with the control. The transcription factor c-fos was up-regulated in hippocampus, and c-jun was elevated both in cortex and hippocampus in PFOS-treated groups. These results indicated that, at least in part, the neurotoxic effect induced by PFOS is mediated by the Ca(2+)-dependent molecules in calcium signaling.
Authors:
Xiaohui Liu; Wei Liu; Yihe Jin; Wenguang Yu; Li Liu; Hongyao Yu
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2010-02-02
Journal Detail:
Title:  Archives of toxicology     Volume:  84     ISSN:  1432-0738     ISO Abbreviation:  Arch. Toxicol.     Publication Date:  2010 Jun 
Date Detail:
Created Date:  2010-05-24     Completed Date:  2010-08-17     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  0417615     Medline TA:  Arch Toxicol     Country:  Germany    
Other Details:
Languages:  eng     Pagination:  471-9     Citation Subset:  IM    
Affiliation:
School of Environmental and Biological Science and Technology, Key Laboratory of Industrial Ecology and Environmental Engineering, Ministry of Education, Dalian University of Technology, Linggong Road 2, 116024, Dalian, China.
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MeSH Terms
Descriptor/Qualifier:
Administration, Oral
Alkanesulfonic Acids / pharmacokinetics,  toxicity*
Animals
Brain / drug effects*,  metabolism
CREB-Binding Protein / genetics,  metabolism
Calcium / metabolism*
Calcium Signaling / drug effects*
Calcium-Calmodulin-Dependent Protein Kinase Type 2 / genetics,  metabolism
Cerebral Cortex / drug effects,  metabolism
Environmental Pollutants / pharmacokinetics,  toxicity*
Fluorocarbons / pharmacokinetics,  toxicity*
Gene Expression / drug effects
Hippocampus / drug effects,  metabolism
Male
Rats
Rats, Sprague-Dawley
Spectrometry, Mass, Electrospray Ionization
Toxicity Tests
Chemical
Reg. No./Substance:
0/Alkanesulfonic Acids; 0/Crebbp protein, rat; 0/Environmental Pollutants; 0/Fluorocarbons; 1763-23-1/perfluorooctane sulfonic acid; 7440-70-2/Calcium; EC 2.3.1.48/CREB-Binding Protein; EC 2.7.11.17/Calcium-Calmodulin-Dependent Protein Kinase Type 2; EC 2.7.11.17/Camk2a protein, rat

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


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