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

2018 · Mixed · Low evidence

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MixedLow evidencePaper 2139

Under user-relevant UMTS exposure conditions (SAR 0.25 to 1.00 W/kg), no DNA damage was detected in comet assays when cells were cultivated with serum. Under serum-free conditions, DNA damage was observed in p53-proficient glioblastoma cells (U87) but not in …

Study snapshot

Publicationmanual · 2018
Study typein_vitro
Reported directionMixed
Evidence ratingLow

Abstract

Mobile phone specific EMF induce transient DNA damage and nucleotide excision repair in serum-deprived human glioblastoma cells Halh Al-Serori, Franziska Ferk, Michael Kundi, Andrea Bileck, Christopher Gerner, Miroslav Mišík, Armen Nersesyan, Monika Waldherr, Manuel Murbach, Tamara T. Lah, Christel Herold-Mende, Andrew R. Collins, Siegfried Knasmülle. Mobile phone specific electromagnetic fields induce transient DNA damage and nucleotide excision repair in serum-deprived human glioblastoma cells. PLOS One. April 12, 2018. doi.org 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. Open access paper: journals.plos.org

Machine Enhanced Logic

AI evidence extraction

Structured fields below were generated from the paper’s abstract and metadata to make the evidence easier to inspect. Automated extraction may be incomplete or incorrect; verify important details against the original paper.

Study typein_vitro
Effect directionmixed
PopulationTen different human cell lines (including brain-derived glioblastoma lines U87 and U251; also lymphocytes, fibroblasts, liver- and buccal tissue-derived cells)
Sample sizeNot supplied
ExposureRF
Evidence strengthLowConfidence: 78% · Peer reviewed: yes

Main findings

Under user-relevant UMTS exposure conditions (SAR 0.25 to 1.00 W/kg), no DNA damage was detected in comet assays when cells were cultivated with serum. Under serum-free conditions, DNA damage was observed in p53-proficient glioblastoma cells (U87) but not in p53-deficient glioblastoma cells (U251); the damage disappeared rapidly and was associated with induced nucleotide excision repair without evidence of double strand breaks.

Outcomes measured

  • DNA damage (single cell gel electrophoresis/comet assay)
  • Nucleotide excision repair (NER) induction
  • Double strand breaks (DSBs)
  • Proteome changes in NER-related proteins
  • γ-interferon pathway activation (limited evidence)

Limitations

  • Frequency and exposure duration not stated in the abstract
  • In vitro study; findings may not generalize to in vivo human exposure
  • Effects depended on cell type and culture conditions (serum-free vs with serum; p53 status)
View raw extracted JSON
{
  "study_type": "in_vitro",
  "exposure": {
    "band": "RF",
    "source": "mobile phone",
    "frequency_mhz": null,
    "sar_wkg": null,
    "duration": null
  },
  "population": "Ten different human cell lines (including brain-derived glioblastoma lines U87 and U251; also lymphocytes, fibroblasts, liver- and buccal tissue-derived cells)",
  "sample_size": null,
  "outcomes": [
    "DNA damage (single cell gel electrophoresis/comet assay)",
    "Nucleotide excision repair (NER) induction",
    "Double strand breaks (DSBs)",
    "Proteome changes in NER-related proteins",
    "γ-interferon pathway activation (limited evidence)"
  ],
  "main_findings": "Under user-relevant UMTS exposure conditions (SAR 0.25 to 1.00 W/kg), no DNA damage was detected in comet assays when cells were cultivated with serum. Under serum-free conditions, DNA damage was observed in p53-proficient glioblastoma cells (U87) but not in p53-deficient glioblastoma cells (U251); the damage disappeared rapidly and was associated with induced nucleotide excision repair without evidence of double strand breaks.",
  "effect_direction": "mixed",
  "limitations": [
    "Frequency and exposure duration not stated in the abstract",
    "In vitro study; findings may not generalize to in vivo human exposure",
    "Effects depended on cell type and culture conditions (serum-free vs with serum; p53 status)"
  ],
  "evidence_strength": "low",
  "confidence": 0.78,
  "peer_reviewed_likely": "yes",
  "keywords": [
    "UMTS",
    "mobile phone",
    "RF-EMF",
    "SAR",
    "glioblastoma",
    "U87",
    "U251",
    "DNA damage",
    "comet assay",
    "nucleotide excision repair",
    "proteomics",
    "p53"
  ],
  "suggested_hubs": [
    {
      "slug": "mobile-phones",
      "weight": 0.9,
      "reason": "Study investigates UMTS (mobile telecommunications) signal exposure in human cell lines at user-relevant SAR."
    }
  ]
}
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AI-extracted fields are generated from the abstract and metadata and may be incomplete or incorrect. This material is for informational purposes and is not medical advice.

Identifiers and source

DOI: 10.1371/journal.pone.0193677
PubMed: Not supplied

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