Effects of a Single Head Exposure to GSM-1800 MHz Signals on the Transcriptome Profile in the Rat Cerebral Cortex: Enhanced Gene Responses Under Proinflammatory Conditions

2020 · Mixed · Low evidence

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MixedLow evidencePaper 1555

Study snapshot

Publicationmanual · 2020

Study typeanimal

Reported directionMixed

Evidence ratingLow

Abstract

Effects of a Single Head Exposure to GSM-1800 MHz Signals on the Transcriptome Profile in the Rat Cerebral Cortex: Enhanced Gene Responses Under Proinflammatory Conditions Lameth J, Arnaud-Cormos D, Lévêque P, Boillée S, Edeline JM, Mallat M. Effects of a Single Head Exposure to GSM-1800 MHz Signals on the Transcriptome Profile in the Rat Cerebral Cortex: Enhanced Gene Responses Under Proinflammatory Conditions. Neurotox Res. 2020 Mar 21. doi: 10.1007/s12640-020-00191-3. Abstract Mobile communications are propagated by electromagnetic fields (EMFs), and since the 1990s, they operate with pulse-modulated signals such as the GSM-1800 MHz. The biological effects of GSM-EMF in humans affected by neuropathological processes remain seldom investigated. In this study, a 2-h head-only exposure to GSM- 1800 MHz was applied to (i) rats undergoing an acute neuroinflammation triggered by a lipopolysaccharide (LPS) treatment, (ii) age-matched healthy rats, or (iii) transgenic hSOD1G93A rats that modeled a presymptomatic phase of human amyotrophic lateral sclerosis (ALS). Gene responses were assessed 24 h after the GSM head- only exposure in a motor area of the cerebral cortex (mCx) where the mean specific absorption rate (SAR) was estimated to be 3.22 W/kg. In LPS-treated rats, a genome-wide mRNA profiling was performed by RNA-seq analysis and revealed significant (adjusted p value < 0.05) but moderate (fold changes < 2) upregulations or downregulations affecting 2.7% of the expressed genes, including genes expressed predominantly in neuronal or in glial cell types and groups of genes involved in protein ubiquitination or dephosphorylation. Reverse transcription-quantitative PCR analyses confirmed gene modulations uncovered by RNA-seq data and showed that in a set of 15 PCR-assessed genes, significant gene responses to GSM-1800 MHz depended upon the acute neuroinflammatory state triggered in LPS-treated rats, because they were not observed in healthy or in hSOD1G93A rats. Together, our data specify the extent of cortical gene modulations triggered by GSM-EMF in the course of an acute neuroinflammation and indicate that GSM-induced gene responses can differ according to pathologies affecting the CNS. ncbi.nlm.nih.gov

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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 typeanimal

Effect directionmixed

PopulationRats: LPS-treated (acute neuroinflammation), age-matched healthy rats, and transgenic hSOD1G93A rats (presymptomatic ALS model)

Sample sizeNot supplied

ExposureRF · 1800 MHz · 3.22 W/kg · 2 h single head-only exposure

Evidence strengthLowConfidence: 78% · Peer reviewed: yes

Main findings

In LPS-treated rats, RNA-seq 24 h after a 2-h GSM-1800 MHz head-only exposure (mean SAR 3.22 W/kg) found significant but moderate (fold changes < 2) up- or downregulation affecting 2.7% of expressed genes. RT-qPCR of 15 genes indicated significant gene responses depended on the acute neuroinflammatory state (present in LPS-treated rats) and were not observed in healthy or hSOD1G93A rats.

Outcomes measured

Genome-wide mRNA expression (RNA-seq) in motor cerebral cortex 24 h post-exposure
RT-qPCR confirmation of selected gene expression changes
Differential gene expression (up/downregulation), including genes related to neuronal/glial cell types and pathways such as protein ubiquitination or dephosphorylation

Limitations

Sample size not reported in the provided abstract/metadata
Single exposure and single post-exposure time point (24 h)
Gene expression changes described as moderate (fold changes < 2)

View raw extracted JSON

{
  "study_type": "animal",
  "exposure": {
    "band": "RF",
    "source": "mobile phone",
    "frequency_mhz": 1800,
    "sar_wkg": 3.22,
    "duration": "2 h single head-only exposure"
  },
  "population": "Rats: LPS-treated (acute neuroinflammation), age-matched healthy rats, and transgenic hSOD1G93A rats (presymptomatic ALS model)",
  "sample_size": null,
  "outcomes": [
    "Genome-wide mRNA expression (RNA-seq) in motor cerebral cortex 24 h post-exposure",
    "RT-qPCR confirmation of selected gene expression changes",
    "Differential gene expression (up/downregulation), including genes related to neuronal/glial cell types and pathways such as protein ubiquitination or dephosphorylation"
  ],
  "main_findings": "In LPS-treated rats, RNA-seq 24 h after a 2-h GSM-1800 MHz head-only exposure (mean SAR 3.22 W/kg) found significant but moderate (fold changes < 2) up- or downregulation affecting 2.7% of expressed genes. RT-qPCR of 15 genes indicated significant gene responses depended on the acute neuroinflammatory state (present in LPS-treated rats) and were not observed in healthy or hSOD1G93A rats.",
  "effect_direction": "mixed",
  "limitations": [
    "Sample size not reported in the provided abstract/metadata",
    "Single exposure and single post-exposure time point (24 h)",
    "Gene expression changes described as moderate (fold changes < 2)"
  ],
  "evidence_strength": "low",
  "confidence": 0.78,
  "peer_reviewed_likely": "yes",
  "keywords": [
    "GSM-1800",
    "1800 MHz",
    "RF-EMF",
    "head-only exposure",
    "specific absorption rate",
    "SAR 3.22 W/kg",
    "rat",
    "cerebral cortex",
    "motor cortex",
    "transcriptome",
    "RNA-seq",
    "RT-qPCR",
    "neuroinflammation",
    "LPS",
    "ALS model",
    "hSOD1G93A"
  ],
  "suggested_hubs": []
}

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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: 10.1007/s12640-020-00191-3
PubMed: Not supplied

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