Gene expression analysis of a human lymphoblastoma cell line exposed in vitro to an intermittent 1.9 GHz pulse-modulated radiofrequency field.
Identifieur interne : 000193 ( Ncbi/Curation ); précédent : 000192; suivant : 000194Gene expression analysis of a human lymphoblastoma cell line exposed in vitro to an intermittent 1.9 GHz pulse-modulated radiofrequency field.
Auteurs : V. Chauhan [Canada] ; A. Mariampillai ; P V Bellier ; S S Qutob ; G B Gajda ; E. Lemay ; A. Thansandote ; J P McnameeSource :
- Radiation research [ 0033-7587 ] ; 2006.
Descripteurs français
- KwdFr :
- Dose de radiation, Exposition environnementale, Humains, Leucémie-lymphome lymphoblastique à précurseurs B et T (anatomopathologie), Leucémie-lymphome lymphoblastique à précurseurs B et T (métabolisme), Lignée cellulaire tumorale, Micro-ondes, Ondes hertziennes, Protéines du choc thermique (métabolisme), Protéines proto-oncogènes (métabolisme), Relation dose-effet des radiations, Réaction de choc thermique (effets des radiations), Régulation de l'expression des gènes tumoraux (effets des radiations), Survie cellulaire (effets des radiations).
- MESH :
- anatomopathologie : Leucémie-lymphome lymphoblastique à précurseurs B et T.
- effets des radiations : Réaction de choc thermique, Régulation de l'expression des gènes tumoraux, Survie cellulaire.
- métabolisme : Leucémie-lymphome lymphoblastique à précurseurs B et T, Protéines du choc thermique, Protéines proto-oncogènes.
- Dose de radiation, Exposition environnementale, Humains, Lignée cellulaire tumorale, Micro-ondes, Ondes hertziennes, Relation dose-effet des radiations.
English descriptors
- KwdEn :
- Cell Line, Tumor, Cell Survival (radiation effects), Dose-Response Relationship, Radiation, Environmental Exposure, Gene Expression Regulation, Neoplastic (radiation effects), Heat-Shock Proteins (metabolism), Heat-Shock Response (radiation effects), Humans, Microwaves, Precursor Cell Lymphoblastic Leukemia-Lymphoma (metabolism), Precursor Cell Lymphoblastic Leukemia-Lymphoma (pathology), Proto-Oncogene Proteins (metabolism), Radiation Dosage, Radio Waves.
- MESH :
- chemical , metabolism : Heat-Shock Proteins, Proto-Oncogene Proteins.
- metabolism : Precursor Cell Lymphoblastic Leukemia-Lymphoma.
- pathology : Precursor Cell Lymphoblastic Leukemia-Lymphoma.
- radiation effects : Cell Survival, Gene Expression Regulation, Neoplastic, Heat-Shock Response.
- Cell Line, Tumor, Dose-Response Relationship, Radiation, Environmental Exposure, Humans, Microwaves, Radiation Dosage, Radio Waves.
Abstract
This study was designed to determine whether radiofrequency (RF) fields of the type used for wireless communications could elicit a cellular stress response. As general indicators of a cellular stress response, we monitored changes in proto-oncogene and heat-shock protein expression. Exponentially growing human lymphoblastoma cells (TK6) were exposed to 1.9 GHz pulse-modulated RF fields at average specific absorption rates (SARs) of 1 and 10 W/kg. Perturbations in the expression levels of the proto-oncogenes FOS, JUN and MYC after exposure to sham and RF fields were assessed by real-time RT-PCR. In addition, the transcript levels of the cellular stress proteins HSP27 and inducible HSP70 were also monitored. We demonstrated that transcript levels of these genes in RF-field-exposed cells showed no significant difference in relation to the sham treatment group. However, concurrent positive (heat-shock) control samples displayed a significant elevation in the expression of HSP27, HSP70, FOS and JUN. Conversely, the levels of MYC mRNA were found to decline in the positive (heat-shock) control. In conclusion, our study found no evidence that the 1.9 GHz RF-field exposure caused a general stress response in TK6 cells under our experimental conditions.
DOI: 10.1667/rr3531.1
PubMed: 16579654
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pubmed:16579654Le document en format XML
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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Cell Line, Tumor</term>
<term>Cell Survival (radiation effects)</term>
<term>Dose-Response Relationship, Radiation</term>
<term>Environmental Exposure</term>
<term>Gene Expression Regulation, Neoplastic (radiation effects)</term>
<term>Heat-Shock Proteins (metabolism)</term>
<term>Heat-Shock Response (radiation effects)</term>
<term>Humans</term>
<term>Microwaves</term>
<term>Precursor Cell Lymphoblastic Leukemia-Lymphoma (metabolism)</term>
<term>Precursor Cell Lymphoblastic Leukemia-Lymphoma (pathology)</term>
<term>Proto-Oncogene Proteins (metabolism)</term>
<term>Radiation Dosage</term>
<term>Radio Waves</term>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr"><term>Dose de radiation</term>
<term>Exposition environnementale</term>
<term>Humains</term>
<term>Leucémie-lymphome lymphoblastique à précurseurs B et T (anatomopathologie)</term>
<term>Leucémie-lymphome lymphoblastique à précurseurs B et T (métabolisme)</term>
<term>Lignée cellulaire tumorale</term>
<term>Micro-ondes</term>
<term>Ondes hertziennes</term>
<term>Protéines du choc thermique (métabolisme)</term>
<term>Protéines proto-oncogènes (métabolisme)</term>
<term>Relation dose-effet des radiations</term>
<term>Réaction de choc thermique (effets des radiations)</term>
<term>Régulation de l'expression des gènes tumoraux (effets des radiations)</term>
<term>Survie cellulaire (effets des radiations)</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Heat-Shock Proteins</term>
<term>Proto-Oncogene Proteins</term>
</keywords>
<keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr"><term>Leucémie-lymphome lymphoblastique à précurseurs B et T</term>
</keywords>
<keywords scheme="MESH" qualifier="effets des radiations" xml:lang="fr"><term>Réaction de choc thermique</term>
<term>Régulation de l'expression des gènes tumoraux</term>
<term>Survie cellulaire</term>
</keywords>
<keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Precursor Cell Lymphoblastic Leukemia-Lymphoma</term>
</keywords>
<keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Leucémie-lymphome lymphoblastique à précurseurs B et T</term>
<term>Protéines du choc thermique</term>
<term>Protéines proto-oncogènes</term>
</keywords>
<keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Precursor Cell Lymphoblastic Leukemia-Lymphoma</term>
</keywords>
<keywords scheme="MESH" qualifier="radiation effects" xml:lang="en"><term>Cell Survival</term>
<term>Gene Expression Regulation, Neoplastic</term>
<term>Heat-Shock Response</term>
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<keywords scheme="MESH" xml:lang="en"><term>Cell Line, Tumor</term>
<term>Dose-Response Relationship, Radiation</term>
<term>Environmental Exposure</term>
<term>Humans</term>
<term>Microwaves</term>
<term>Radiation Dosage</term>
<term>Radio Waves</term>
</keywords>
<keywords scheme="MESH" xml:lang="fr"><term>Dose de radiation</term>
<term>Exposition environnementale</term>
<term>Humains</term>
<term>Lignée cellulaire tumorale</term>
<term>Micro-ondes</term>
<term>Ondes hertziennes</term>
<term>Relation dose-effet des radiations</term>
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<front><div type="abstract" xml:lang="en">This study was designed to determine whether radiofrequency (RF) fields of the type used for wireless communications could elicit a cellular stress response. As general indicators of a cellular stress response, we monitored changes in proto-oncogene and heat-shock protein expression. Exponentially growing human lymphoblastoma cells (TK6) were exposed to 1.9 GHz pulse-modulated RF fields at average specific absorption rates (SARs) of 1 and 10 W/kg. Perturbations in the expression levels of the proto-oncogenes FOS, JUN and MYC after exposure to sham and RF fields were assessed by real-time RT-PCR. In addition, the transcript levels of the cellular stress proteins HSP27 and inducible HSP70 were also monitored. We demonstrated that transcript levels of these genes in RF-field-exposed cells showed no significant difference in relation to the sham treatment group. However, concurrent positive (heat-shock) control samples displayed a significant elevation in the expression of HSP27, HSP70, FOS and JUN. Conversely, the levels of MYC mRNA were found to decline in the positive (heat-shock) control. In conclusion, our study found no evidence that the 1.9 GHz RF-field exposure caused a general stress response in TK6 cells under our experimental conditions.</div>
</front>
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