Melatonin and omega-3 neuroprotection in prenatal rat spinal cord exposed to 900 MHz electromagnetic field.

Biomolecules & biomedicine · 2025 · Mixed · Low evidence

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MixedLow evidencePaper 5890

Across groups, no significant differences were observed for GM/WM volume ratios, GM/total volume ratios, WM/total volume ratios, or total spinal cord volume (p>0.05). Motor neuron numbers were significantly reduced in the EMF-ω3 group versus control (p<0.01).…

Study snapshot

PublicationBiomolecules & biomedicine · 2025
Study typeanimal
Reported directionMixed
Evidence ratingLow

Abstract

The electromagnetic field (EMF) emitted by electronic devices induces pathological changes in tissues, adversely affecting embryonic and pubertal development. This study investigates the effects of melatonin (Mel) and omega-3 fatty acids (ω3) on the spinal cord in rats exposed to EMF, employing stereological methods alongside light and electron microscopic evaluations. Pregnant Wistar albino rats were divided into seven groups: Control (CONT), sham-exposed (SHAM), EMF alone, EMF-Mel, EMF-ω3, Mel only, and ω3 only. The EMF, EMF-Mel, and EMF-ω3 groups were exposed to a 900 MHz EMF for two hours daily during the prenatal period (21 days). Mel and ω3 were administered via intragastric gavage prior to EMF exposure. Upon completion of the experiment (on the 35th day post-birth), spinal cord tissues of all male offspring were dissected and subjected to light and ultrastructural examinations. Stereological analyses calculated grey matter (GM) to total volume ratios, white matter (WM) to total volume ratios, GM to WM volume ratios, total spinal cord volume, and motor neuron counts. No significant differences were observed among the groups regarding GM/WM volume ratios, GM/total volume ratios, WM/total volume ratios, and total spinal cord volume (p > 0.05). However, a significant reduction in motor neuron numbers was noted in the EMF-ω3 group compared to the CONT group (p < 0.01). Light and ultrastructural examinations revealed marked motor neuron degeneration and axonal disruption in the EMF group, which were mitigated in the Mel and ω3-treated groups. These findings indicate that prenatal exposure to 900 MHz EMF exerts detrimental effects on spinal cord tissue and underscore the necessity for further studies exploring varying doses and durations to elucidate the potential effects of ω3 and Mel.

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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
PopulationPregnant Wistar albino rats and male offspring (spinal cord assessed on postnatal day 35)
Sample sizeNot supplied
ExposureRF · 900 MHz · 2 hours daily during prenatal period (21 days)
Evidence strengthLowConfidence: 74% · Peer reviewed: yes

Main findings

Across groups, no significant differences were observed for GM/WM volume ratios, GM/total volume ratios, WM/total volume ratios, or total spinal cord volume (p>0.05). Motor neuron numbers were significantly reduced in the EMF-ω3 group versus control (p<0.01). Light and ultrastructural examinations showed marked motor neuron degeneration and axonal disruption in the EMF group, which were mitigated in melatonin- and ω3-treated groups.

Outcomes measured

  • Spinal cord grey matter (GM)/white matter (WM) volume ratios
  • GM/total volume ratio
  • WM/total volume ratio
  • Total spinal cord volume
  • Motor neuron counts
  • Light microscopic spinal cord morphology
  • Ultrastructural (electron microscopy) spinal cord morphology (motor neuron degeneration, axonal disruption)

Limitations

  • Sample size not reported in abstract
  • Exposure metric (e.g., SAR) not reported
  • Only male offspring assessed
  • Single frequency (900 MHz) and single exposure schedule studied
  • Findings include an unexpected reduction in motor neuron numbers in EMF-ω3 vs control despite reported morphological mitigation
View raw extracted JSON
{
  "study_type": "animal",
  "exposure": {
    "band": "RF",
    "source": "electronic devices",
    "frequency_mhz": 900,
    "sar_wkg": null,
    "duration": "2 hours daily during prenatal period (21 days)"
  },
  "population": "Pregnant Wistar albino rats and male offspring (spinal cord assessed on postnatal day 35)",
  "sample_size": null,
  "outcomes": [
    "Spinal cord grey matter (GM)/white matter (WM) volume ratios",
    "GM/total volume ratio",
    "WM/total volume ratio",
    "Total spinal cord volume",
    "Motor neuron counts",
    "Light microscopic spinal cord morphology",
    "Ultrastructural (electron microscopy) spinal cord morphology (motor neuron degeneration, axonal disruption)"
  ],
  "main_findings": "Across groups, no significant differences were observed for GM/WM volume ratios, GM/total volume ratios, WM/total volume ratios, or total spinal cord volume (p>0.05). Motor neuron numbers were significantly reduced in the EMF-ω3 group versus control (p<0.01). Light and ultrastructural examinations showed marked motor neuron degeneration and axonal disruption in the EMF group, which were mitigated in melatonin- and ω3-treated groups.",
  "effect_direction": "mixed",
  "limitations": [
    "Sample size not reported in abstract",
    "Exposure metric (e.g., SAR) not reported",
    "Only male offspring assessed",
    "Single frequency (900 MHz) and single exposure schedule studied",
    "Findings include an unexpected reduction in motor neuron numbers in EMF-ω3 vs control despite reported morphological mitigation"
  ],
  "evidence_strength": "low",
  "confidence": 0.74,
  "peer_reviewed_likely": "yes",
  "keywords": [
    "900 MHz",
    "RF-EMF",
    "prenatal exposure",
    "rat",
    "spinal cord",
    "motor neuron",
    "melatonin",
    "omega-3",
    "stereology",
    "electron microscopy"
  ],
  "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: 10.17305/bb.2025.12633
PubMed: 40694058

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