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

Author: Al-Serori H1, Ferk F1, Kundi M2, Bileck A3, Gerner C3, Mišík M1, Nersesyan A1, Waldherr M1, Murbach M4, Lah TT5, Herold-Mende C6, Collins AR7, Knasmüller S1
1Institute of Cancer Research, Department of Internal Medicine 1, Medical University of Vienna, Vienna, Austria.
2Center for Public Health, Department of Environmental Health, Medical University of Vienna, Vienna, Austria.
3Department of Analytical Chemistry, Faculty of Chemistry, University of Vienna, Vienna, Austria.
4IT 'IS Foundation, Zurich, Switzerland.
5Department of Genetic Toxicology and Cancer Biology, National Institute of Biology, Ljubljana, Slovenia.
6Experimental Neurosurgery, Department of Neurosurgery, University of Heidelberg, Heidelberg, Germany.
7Department of Nutrition, University of Oslo, Oslo, Norway.
Conference/Journal: PLoS One.
Date published: 2018 Apr 12
Other: Volume ID: 13 , Issue ID: 4 , Pages: e0193677 , Special Notes: doi: 10.1371/journal.pone.0193677. eCollection 2018. , Word Count: 219

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.

PMID: 29649215 DOI: 10.1371/journal.pone.0193677