Neurotoxic effects of 3.5 GHz GSM-like RF exposure on cultured DRG neurons: a mechanistic insight into oxidative and apoptotic pathways

Int J Radiat Biol · 2026 · Harm · Low evidence

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HarmLow evidencePaper 2453

In primary mouse DRG cultures, pulsed 3.5 GHz GSM-like RF-EMF exposure (non-thermal; <0.1 °C temperature difference) produced a significant time-dependent reduction in cell viability and increased ROS. Mitochondrial-apoptotic signaling markers shifted toward …

Study snapshot

PublicationInt J Radiat Biol · 2026
Study typein_vitro
Reported directionHarm
Evidence ratingLow

Abstract

Category: Neuroscience Tags: RF-EMF, neurotoxicity, oxidative stress, apoptosis, dorsal root ganglion, 3.5 GHz, electromagnetic fields DOI: 10.1080/09553002.2026.2617592 URL: pubmed.ncbi.nlm.nih.gov Overview This study explored the effects of strictly non-thermal, GSM-like 3.5 GHz radiofrequency electromagnetic fields (RF-EMF)—with frequencies overlapping those used by 5G networks—on peripheral sensory neurons. Specifically, researchers examined if such exposures disrupt redox balance and activate apoptotic processes in mouse dorsal root ganglion (DRG) neurons. Materials and Methods - Mouse DRG cultures were exposed to pulsed 3.5 GHz RF-EMF (217 Hz, ~12.5% duty cycle) for periods from 1 to 24 hours in a specialized GTEM-based setup. - Exposure conditions maintained a temperature difference below 0.1°C to ensure non-thermal exposure, supported by precise dosimetry consistent with IEEE/IEC guidelines. - Outcomes measured included cell viability, levels of reactive oxygen species (ROS), mitochondrial apoptotic markers (e.g., Bax, Bcl-2, cytochrome c, caspase-3), and the neurotrophin receptor p75NTR, analyzed via blinded confocal microscopy. Findings - RF-EMF exposure induced a significant and time-dependent reduction in cell viability. - Robust increases in ROS were observed along with upregulation of pro-apoptotic markers (Bax and caspase-3) and release of cytochrome c. - Anti-apoptotic Bcl-2 levels decreased and p75NTR was upregulated, indicating maladaptive neurotrophin signaling. - Maximal effects occurred at 12–24 hours post-exposure. - SAR values: total 171 mW/kg; 1-g 270 mW/kg; peak 1149 mW/kg, all under non-thermal conditions. Conclusion The results demonstrate that non-thermal 3.5 GHz RF-EMF disrupts redox homeostasis and initiates mitochondria-mediated apoptosis in peripheral sensory neurons. This provides mechanistic evidence of peripheral neuronal vulnerability associated with mid-band RF exposures and strengthens the connection between RF-EMF exposure and adverse neurobiological outcomes, underscoring the need for further in vivo investigation to assess long-term impacts on health.

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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 typein_vitro
Effect directionharm
PopulationPrimary mouse dorsal root ganglion (DRG) neuron cultures
Sample sizeNot supplied
ExposureRF · 3500 MHz · 1–24 h
Evidence strengthLowConfidence: 78% · Peer reviewed: yes

Main findings

In primary mouse DRG cultures, pulsed 3.5 GHz GSM-like RF-EMF exposure (non-thermal; <0.1 °C temperature difference) produced a significant time-dependent reduction in cell viability and increased ROS. Mitochondrial-apoptotic signaling markers shifted toward apoptosis (increased Bax and caspase-3, decreased Bcl-2, cytochrome c release), with maximal effects at 12–24 h, and p75^NTR was upregulated.

Outcomes measured

  • Cell viability
  • Reactive oxygen species (ROS)
  • Bax
  • Bcl-2
  • Cytochrome c release
  • Caspase-3
  • p75^NTR

Limitations

  • In vitro primary culture model; findings may not translate to in vivo outcomes
  • No sample size reported in the abstract
  • Specific absorption rate (SAR) not reported in the abstract
  • Exposure described as overlapping 5G mid-band frequencies but not using a 5G NR waveform; generalizability to real-world 5G signals is unclear
View raw extracted JSON
{
  "study_type": "in_vitro",
  "exposure": {
    "band": "RF",
    "source": null,
    "frequency_mhz": 3500,
    "sar_wkg": null,
    "duration": "1–24 h"
  },
  "population": "Primary mouse dorsal root ganglion (DRG) neuron cultures",
  "sample_size": null,
  "outcomes": [
    "Cell viability",
    "Reactive oxygen species (ROS)",
    "Bax",
    "Bcl-2",
    "Cytochrome c release",
    "Caspase-3",
    "p75^NTR"
  ],
  "main_findings": "In primary mouse DRG cultures, pulsed 3.5 GHz GSM-like RF-EMF exposure (non-thermal; <0.1 °C temperature difference) produced a significant time-dependent reduction in cell viability and increased ROS. Mitochondrial-apoptotic signaling markers shifted toward apoptosis (increased Bax and caspase-3, decreased Bcl-2, cytochrome c release), with maximal effects at 12–24 h, and p75^NTR was upregulated.",
  "effect_direction": "harm",
  "limitations": [
    "In vitro primary culture model; findings may not translate to in vivo outcomes",
    "No sample size reported in the abstract",
    "Specific absorption rate (SAR) not reported in the abstract",
    "Exposure described as overlapping 5G mid-band frequencies but not using a 5G NR waveform; generalizability to real-world 5G signals is unclear"
  ],
  "evidence_strength": "low",
  "confidence": 0.78,
  "peer_reviewed_likely": "yes",
  "keywords": [
    "3.5 GHz",
    "RF-EMF",
    "GSM-like",
    "non-thermal",
    "DRG neurons",
    "oxidative stress",
    "ROS",
    "mitochondrial apoptosis",
    "Bax",
    "Bcl-2",
    "cytochrome c",
    "caspase-3",
    "p75NTR",
    "GTEM",
    "pulsed exposure",
    "mid-band"
  ],
  "suggested_hubs": [
    {
      "slug": "5g-policy",
      "weight": 0.32,
      "reason": "Exposure frequency overlaps bands used by 5G networks (3.5 GHz), though waveform is not 5G NR."
    }
  ]
}
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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: 10.1080/09553002.2026.2617592
PubMed: 41562640

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