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Mobile phone specific electromagnetic fields induce transient DNA damage and nucleotide excision repair in serum-deprived human glioblastoma cells

Authors :
Christopher Gerner
Halh Al-Serori
Franziska Ferk
Tamara T. Lah
Monika Waldherr
Siegfried Knasmüller
Andrew Collins
Miroslav Mišík
Christel Herold-Mende
Andrea Bileck
Armen Nersesyan
Michael Kundi
Manuel Murbach
Source :
PLoS ONE, 13 (4), PLoS ONE, Vol 13, Iss 4, p e0193677 (2018), PLoS ONE
Publication Year :
2018
Publisher :
PLOS, 2018.

Abstract

Some epidemiological studies indicate that the use of mobile phones causes cancer in humans (in particular glioblastomas). It is known that DNA damage plays a key role in malignant transformation; therefore, we investigated the impact of the UMTS signal which is widely used in mobile telecommunications, on DNA stability in ten different human cell lines (six brain derived cell lines, lymphocytes, fibroblasts, liver and buccal tissue derived cells) under conditions relevant for users (SAR 0.25 to 1.00 W/kg). We found no evidence for induction of damage in single cell gel electrophoresis assays when the cells were cultivated with serum. However, clear positive effects were seen in a p53 proficient glioblastoma line (U87) when the cells were grown under serum free conditions, while no effects were found in p53 deficient glioblastoma cells (U251). Further experiments showed that the damage disappears rapidly in U87 and that exposure induced nucleotide excision repair (NER) and does not cause double strand breaks (DSBs). The observation of NER induction is supported by results of a proteome analysis indicating that several proteins involved in NER are up-regulated after exposure to UMTS; additionally, we found limited evidence for the activation of the γ-interferon pathway. The present findings show that the signal causes transient genetic instability in glioma derived cells and activates cellular defense systems.<br />PLoS ONE, 13 (4)<br />ISSN:1932-6203

Details

Language :
English
ISSN :
19326203
Database :
OpenAIRE
Journal :
PLoS ONE, 13 (4), PLoS ONE, Vol 13, Iss 4, p e0193677 (2018), PLoS ONE
Accession number :
edsair.doi.dedup.....ca1b843a39c8e5c252e41535fde8bb20