Document Detail


Subchronic exposure of hsp70.1-deficient mice to radiofrequency radiation.
MedLine Citation:
PMID:  16449085     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
PURPOSE: Heat shock protein 70 (HSP70) is one of the most inducible proteins to play a cytoprotective role under stressful conditions. Previously we generated hsp70.1-deficient mice to elucidate the in vivo function of HSP70 in detail. The renal tissues and embryonic fibroblasts of these mice were shown to be more vulnerable to hyperosmotic stress. Since RF (radiofrequency) energy has been suggested to be an environmental stressor, we carried out a study to determine whether sub-chronic RF exposure can cause constitutive induction of a stress response at a cellular and/or molecular level in hsp70.1-deficient mice due to repeated stimulation. MATERIALS AND METHODS: Eight-week-old hsp70.1-deficient mice were exposed twice daily for 45 min, with a 15 min interval, 5 days a week for 10 weeks. Whole-body average specific absorption rate was 0.4 W/Kg for fields of both 849 MHz and 1763 MHz. Major tissues were histopathologically analysed, and immunocytochemically evaluated for cell proliferative activity. Apoptosis was investigated by TdT-mediated dUTP nick-end labeling (TUNEL) assay. To determine whether RF radiation elicits a stress response, the expression level of heat shock proteins (HSP) and phosphorylation of the stress-activated kinases were also observed by western blots. RESULTS: No difference was observed in the histopathological analysis between sham- and RF-exposed mice. There was no evidence of increased proliferative and apoptotic activities. The levels of HSP90, HSP70, and HSP25 showed no obvious changes. RF exposure did not affect the phosphorylation status of the major stress-activated kinase (MAPK); extracellular signal-regulated kinase 1/2 (ERK1/2), C-Jun N-terminal kinase 1/2 (JNK1/2) or p38 MAPK. CONCLUSION: The hsp70.1-deficient mice did not show any significant changes in terms of cell proliferation, apoptosis, or stress response due to exposure of 849 or 1,763 MHz RF fields.
Authors:
Jae-Seon Lee; Tai-Qin Huang; Je-Jung Lee; Jeong-Ki Pack; Ja-June Jang; Jeong-Sun Seo
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  International journal of radiation biology     Volume:  81     ISSN:  0955-3002     ISO Abbreviation:  Int. J. Radiat. Biol.     Publication Date:  2005 Oct 
Date Detail:
Created Date:  2006-02-01     Completed Date:  2006-04-18     Revised Date:  2009-11-19    
Medline Journal Info:
Nlm Unique ID:  8809243     Medline TA:  Int J Radiat Biol     Country:  England    
Other Details:
Languages:  eng     Pagination:  781-92     Citation Subset:  IM; S    
Affiliation:
Laboratory of Functional Genomics, Korea Institute of Radiological & Medical Sciences, Seoul.
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MeSH Terms
Descriptor/Qualifier:
Animals
Apoptosis / radiation effects*
Cell Proliferation / radiation effects*
Female
HSP70 Heat-Shock Proteins / genetics*
Immunohistochemistry
In Situ Nick-End Labeling
Male
Mice
Mitogen-Activated Protein Kinase Kinases / metabolism
Phosphorylation
Radiation Injuries*
Chemical
Reg. No./Substance:
0/HSP70 Heat-Shock Proteins; 0/heat-shock protein 70.1; EC 2.7.12.2/Mitogen-Activated Protein Kinase Kinases

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


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