Mitigation of 3.5 GHz Electromagnetic Field-Induced BV2 Microglial Cytotoxicity by Polydeoxyribonucleotide

Current Issues in Molecular Biology · 2025 · Harm · Low evidence

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HarmLow evidencePaper 2619

Study snapshot

PublicationCurrent Issues in Molecular Biology · 2025

Study typein_vitro

Reported directionHarm

Evidence ratingLow

Abstract

Category: Cellular Neuroscience, Molecular Biology Tags: electromagnetic fields, microglial cytotoxicity, 3.5 GHz, PDRN, oxidative stress, apoptosis, 5G radiation DOI: 10.3390/cimb47060386 URL: mdpi.com Overview Emerging evidence highlights the biological risks associated with electromagnetic fields (EMFs) generated by electronic devices. However, our understanding of the toxic effects and underlying mechanisms induced by EMF exposure on microglial cells is limited. The identification of potential natural inhibitors to mitigate these effects is of increasing importance, especially with the widespread use of devices like smartphones (5G) and microwave ovens emitting 3.5 GHz EMF radiation. Study Focus - Examined the effects of 3.5 GHz EMF radiation on the growth of BV2 mouse microglial cells. - Evaluated the ability of polydeoxyribonucleotide (PDRN), a DNA preparation from salmon sperm, to inhibit these effects. Findings - Exposure to 3.5 GHz EMF radiation for 2 hours significantly inhibited cell growth and triggered apoptosis in BV2 cells. - Markers of cytotoxicity included reduced cell survival, increased genomic DNA fragmentation, heightened reactive oxygen species (ROS) levels, and changes in phosphorylation and expression of signaling proteins (JNK-1/2, p38 MAPK, ERK-1/2, eIF-2a, procaspase-9). - Pharmacological studies pinpointed JNK-1/2, p38 MAPK activation, and ROS generation as key events in EMF-induced cytotoxicity. - PDRN effectively countered EMF-induced cytotoxicity by inhibiting JNK-1/2, p38 MAPK, caspase-9 activation, and ROS production, though it did not impact eIF-2 phosphorylation. Conclusion This study is the first to demonstrate that PDRN protects BV2 microglial cells against cytotoxicity induced by 3.5 GHz EMF exposure—a frequency commonly emitted by modern wireless devices and appliances. PDRN's protective effects are mainly exerted through modulation of ROS, JNK-1/2, p38 MAPK, and caspase-9. This highlights a direct biological link between EMF exposure and cellular damage, confirming the connection to health risk, and underscores the need for protective strategies in environments with significant EMF exposure.

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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

PopulationBV2 mouse microglial cells

Sample sizeNot supplied

ExposureRF · 3500 MHz · 2 hours

Evidence strengthLowConfidence: 78% · Peer reviewed: yes

Main findings

Exposure to 3.5 GHz EMF for 2 hours significantly inhibited BV2 cell growth and induced cytotoxicity/apoptosis, including reduced survival, increased DNA fragmentation, elevated ROS, and changes in signaling proteins (e.g., JNK-1/2, p38 MAPK, ERK-1/2, eIF-2α, procaspase-9). Pharmacological studies implicated ROS generation and JNK-1/2 and p38 MAPK activation as key events. Polydeoxyribonucleotide (PDRN) countered EMF-induced cytotoxicity by inhibiting ROS production and JNK-1/2, p38 MAPK, and caspase-9 activation, without affecting eIF-2 phosphorylation.

Outcomes measured

cell growth
cell survival
apoptosis
genomic DNA fragmentation
reactive oxygen species (ROS)
JNK-1/2 signaling
p38 MAPK signaling
ERK-1/2 signaling
eIF-2α phosphorylation
procaspase-9/caspase-9 activation

Limitations

In vitro study in a mouse microglial cell line (BV2); generalizability to humans or in vivo conditions not stated.
Exposure metric details (e.g., SAR, power density) not provided in the abstract.
Sample size and replication details not provided in the abstract.

View raw extracted JSON

{
  "study_type": "in_vitro",
  "exposure": {
    "band": "RF",
    "source": "wireless devices/appliances (e.g., smartphones (5G), microwave ovens)",
    "frequency_mhz": 3500,
    "sar_wkg": null,
    "duration": "2 hours"
  },
  "population": "BV2 mouse microglial cells",
  "sample_size": null,
  "outcomes": [
    "cell growth",
    "cell survival",
    "apoptosis",
    "genomic DNA fragmentation",
    "reactive oxygen species (ROS)",
    "JNK-1/2 signaling",
    "p38 MAPK signaling",
    "ERK-1/2 signaling",
    "eIF-2α phosphorylation",
    "procaspase-9/caspase-9 activation"
  ],
  "main_findings": "Exposure to 3.5 GHz EMF for 2 hours significantly inhibited BV2 cell growth and induced cytotoxicity/apoptosis, including reduced survival, increased DNA fragmentation, elevated ROS, and changes in signaling proteins (e.g., JNK-1/2, p38 MAPK, ERK-1/2, eIF-2α, procaspase-9). Pharmacological studies implicated ROS generation and JNK-1/2 and p38 MAPK activation as key events. Polydeoxyribonucleotide (PDRN) countered EMF-induced cytotoxicity by inhibiting ROS production and JNK-1/2, p38 MAPK, and caspase-9 activation, without affecting eIF-2 phosphorylation.",
  "effect_direction": "harm",
  "limitations": [
    "In vitro study in a mouse microglial cell line (BV2); generalizability to humans or in vivo conditions not stated.",
    "Exposure metric details (e.g., SAR, power density) not provided in the abstract.",
    "Sample size and replication details not provided in the abstract."
  ],
  "evidence_strength": "low",
  "confidence": 0.78,
  "peer_reviewed_likely": "yes",
  "keywords": [
    "3.5 GHz",
    "RF-EMF",
    "5G",
    "BV2",
    "microglia",
    "cytotoxicity",
    "apoptosis",
    "oxidative stress",
    "ROS",
    "JNK",
    "p38 MAPK",
    "PDRN",
    "polydeoxyribonucleotide"
  ],
  "suggested_hubs": [
    {
      "slug": "5g-policy",
      "weight": 0.62,
      "reason": "Study explicitly references 3.5 GHz and '5G radiation' in tags and context."
    }
  ]
}

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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: 10.3390/cimb47060386
PubMed: Not supplied

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