Melatonin ameliorates RF-EMR-induced reproductive damage by inhibiting ferroptosis through Nrf2 pathway activation

PAPER manual Pathology Research and Practice 2025 Animal study Effect: harm Evidence: Low

Read original paper → DOI: 10.1016/j.prp.2025.156003 PMID: 40344840 Evidence Lab

Abstract

Category: Reproductive Toxicology Tags: RF-EMR, melatonin, ferroptosis, Nrf2 pathway, oxidative stress, male reproduction, fertility DOI: 10.1016/j.prp.2025.156003 URL: pubmed.ncbi.nlm.nih.gov Overview In recent years, growing evidence has highlighted significant concerns regarding the hazardous effects of radiofrequency electromagnetic radiation (RF-EMR) on male reproductive function. The search for viable protective agents to counteract these effects has brought attention to melatonin, known for its antioxidant and anti-apoptotic properties and its role in reproductive health. Yet, the molecular pathways through which melatonin shields against RF-EMR-induced reproductive damage have remained elusive. Findings - Prolonged exposure (8 weeks) to RF-EMR (2.45 GHz; power density 2.5 W/m2; SAR 0.125-0.5 W/kg) led to increased oxidative stress and ferroptosis in testicular tissue of male mice. - The resulting oxidative damage from RF-EMR caused notable decreases in sperm quality. - Administering melatonin notably reduced the testicular oxidative injury and inhibited ferroptosis induced by RF-EMR. - Mechanistic studies demonstrated that melatonin counters reactive oxygen species (ROS) production and ferroptosis by activating the Nrf2 signaling pathway through MT1/MT2 receptors. Conclusion RF-EMR exposure is directly linked to harmful effects on male reproduction, primarily via ferroptosis in testicular tissue. Melatonin substantially protects against this RF-EMR-induced damage by activating the Nrf2 pathway, thereby suppressing ferroptosis. These results underscore the potential of melatonin as a therapeutic agent for male infertility linked to RF-EMR exposure. Further controlled trials are recommended to assess melatonin’s clinical benefit in addressing male reproductive damage caused by electromagnetic fields.

AI evidence extraction

At a glance

Study type

Animal study

Effect direction

harm

Population

Male mice

Sample size

—

Exposure

microwave · 2450 MHz · 8 weeks

Evidence strength

Low

Confidence: 78% · Peer-reviewed: yes

Main findings

Prolonged RF-EMR exposure (2.45 GHz; power density 2.5 W/m2; SAR 0.125–0.5 W/kg) for 8 weeks increased oxidative stress and ferroptosis in male mouse testicular tissue and was associated with decreased sperm quality. Melatonin administration reduced testicular oxidative injury and inhibited RF-EMR-induced ferroptosis, with mechanistic evidence suggesting activation of the Nrf2 pathway via MT1/MT2 receptors.

Outcomes measured

Oxidative stress in testicular tissue
Ferroptosis in testicular tissue
Sperm quality
ROS production
Nrf2 signaling pathway activation (via MT1/MT2 receptors)

Limitations

Sample size not reported in provided abstract/metadata
Exposure source (e.g., Wi‑Fi router vs other generator) not specified
Details of melatonin dosing/regimen not provided in provided abstract/metadata
Animal model; clinical relevance to humans not established in provided abstract/metadata

View raw extracted JSON

{
    "study_type": "animal",
    "exposure": {
        "band": "microwave",
        "source": null,
        "frequency_mhz": 2450,
        "sar_wkg": null,
        "duration": "8 weeks"
    },
    "population": "Male mice",
    "sample_size": null,
    "outcomes": [
        "Oxidative stress in testicular tissue",
        "Ferroptosis in testicular tissue",
        "Sperm quality",
        "ROS production",
        "Nrf2 signaling pathway activation (via MT1/MT2 receptors)"
    ],
    "main_findings": "Prolonged RF-EMR exposure (2.45 GHz; power density 2.5 W/m2; SAR 0.125–0.5 W/kg) for 8 weeks increased oxidative stress and ferroptosis in male mouse testicular tissue and was associated with decreased sperm quality. Melatonin administration reduced testicular oxidative injury and inhibited RF-EMR-induced ferroptosis, with mechanistic evidence suggesting activation of the Nrf2 pathway via MT1/MT2 receptors.",
    "effect_direction": "harm",
    "limitations": [
        "Sample size not reported in provided abstract/metadata",
        "Exposure source (e.g., Wi‑Fi router vs other generator) not specified",
        "Details of melatonin dosing/regimen not provided in provided abstract/metadata",
        "Animal model; clinical relevance to humans not established in provided abstract/metadata"
    ],
    "evidence_strength": "low",
    "confidence": 0.7800000000000000266453525910037569701671600341796875,
    "peer_reviewed_likely": "yes",
    "keywords": [
        "RF-EMR",
        "2.45 GHz",
        "microwave",
        "melatonin",
        "ferroptosis",
        "Nrf2 pathway",
        "oxidative stress",
        "male reproduction",
        "fertility",
        "testis",
        "sperm quality",
        "MT1",
        "MT2"
    ],
    "suggested_hubs": []
}

AI can be wrong. Always verify against the paper.

AI-extracted fields are generated from the abstract/metadata and may be incomplete or incorrect. This content is for informational purposes only and is not medical advice.

Comments

No comments yet.