title: Phosphorylation and gene expression of p53 are not affected in human cells exposed to 2.1425 GHz band CW or W-CDMA modulated radiation allocated to mobile radio base stations.
abstract: A large-scale in vitro study focusing on low-level radiofrequency (RF) fields from mobile radio base stations employing the International Mobile Telecommunication 2000 (IMT-2000) cellular system was conducted to test the hypothesis that modulated RF fields induce apoptosis or other cellular stress response that activate p53 or the p53-signaling pathway. First, we evaluated the response of human cells to microwave exposure at a specific absorption rate (SAR) of 80 mW/kg, which corresponds to the limit of the average whole-body SAR for general public exposure defined as a basic restriction by the International Commission on Non-Ionizing Radiation Protection (ICNIRP) guidelines. Second, we investigated whether continuous wave (CW) and wideband code division multiple access (W-CDMA) modulated signal RF fields at 2.1425 GHz induced apoptosis or any signs of stress. Human glioblastoma A172 cells were exposed to W-CDMA radiation at SARs of 80, 250, and 800 mW/kg, and CW radiation at 80 mW/kg for 24 or 48 h. Human IMR-90 fibroblasts from fetal lungs were exposed to both W-CDMA and CW radiation at a SAR of 80 mW/kg for 28 h. Under the RF field exposure conditions described above, no significant differences in the percentage of apoptotic cells were observed between the test groups exposed to RF signals and the sham-exposed negative controls, as evaluated by the Annexin V affinity assay. No significant differences in expression levels of phosphorylated p53 at serine 15 or total p53 were observed between the test groups and the negative controls by the bead-based multiplex assay. Moreover, microarray hybridization and real-time RT-PCR analysis showed no noticeable differences in gene expression of the subsequent downstream targets of p53 signaling involved in apoptosis between the test groups and the negative controls. Our results confirm that exposure to low-level RF signals up to 800 mW/kg does not induce p53-dependent apoptosis, DNA damage, or other stress response in human cells.
authors.affiliation: Research Division for Advanced Technology, Kashima Laboratory, Mitsubishi Chemical Safety Institute Ltd., Kamisu, Japan. h-hirose@ankaken.co.jp
authors.forename: H
authors.initials: H
authors.lastname: Hirose
authors.forename: N
authors.initials: N
authors.lastname: Sakuma
authors.forename: N
authors.initials: N
authors.lastname: Kaji
authors.forename: T
authors.initials: T
authors.lastname: Suhara
authors.forename: M
authors.initials: M
authors.lastname: Sekijima
authors.forename: T
authors.initials: T
authors.lastname: Nojima
authors.forename: J
authors.initials: J
authors.lastname: Miyakoshi
mesh_terms: D000595:Amino Acid Sequence; D017209:Apoptosis / Q000528:radiation effects; D002460:Cell Line; D045744:Cell Line, Tumor; D005347:Fibroblasts / Q000528:radiation effects; D015870:Gene Expression / Q000528:radiation effects*; D005909:Glioblastoma; D006801:Humans; D020411:Oligonucleotide Array Sequence Analysis; D010766:Phosphorylation / Q000528:radiation effects; D011846:Radio Waves; D012694:Serine / Q000378:metabolism; D016159:Tumor Suppressor Protein p53 / Q000096:biosynthesis* / Q000528:radiation effects
chemical_list: D016159:Tumor Suppressor Protein p53; D012694:Serine