Doxorubicin-induced cardiotoxicity under 28 GHz 5G-band electromagnetic radiation in rats: Insights into the mitigative role of vitamin C

Abstract

Category: Toxicology, Cardiology, Bioelectromagnetics Tags: cardiotoxicity, 5G, electromagnetic radiation, vitamin C, doxorubicin, oxidative stress, apoptosis DOI: 10.1016/j.taap.2025.117703 URL: pubmed.ncbi.nlm.nih.gov Overview Doxorubicin (DOX), an effective anthracycline chemotherapeutic agent, induces cardiotoxicity through oxidative stress, mitochondrial dysfunction, and activation of apoptotic pathways. As millimeter-wave frequencies used in fifth-generation (5G) communication systems continue to expand, experimental data on potential biological interactions under clinically relevant conditions remain limited. This study investigated whether short-term 28-GHz electromagnetic radiation (EMR) modifies the cardiac response to DOX and evaluated the potential protective role of vitamin C. - Thirty male Sprague-Dawley rats were assigned to five groups (n = 6): Sham, DOX, DOX + Vit C, DOX + 5G, and DOX + 5G + Vit C. - DOX (15 mg/kg intraperitoneally, six injections) induced cardiotoxicity, while vitamin C (250 mg/kg orally) was administered daily for 14 days. - EMR exposure consisted of three 10-min cycles per day at 28 GHz for 14 days. Findings - Cardiac injury was assessed using electrocardiography, serum cTnI, oxidative markers (MDA, GSH, SOD, CAT), apoptotic and inflammatory gene expression (BAX, CASP3, BCL-2, TNF-a), and design-based stereology. - DOX induced significant functional, biochemical, molecular, and structural alterations. - Co-exposure to 28-GHz EMR amplified reductions in CAT (p < 0.001), and enhanced pro-apoptotic BAX gene expression (p < 0.0001), accompanied by QT interval prolongation (p < 0.05). - Vitamin C provided partial protection across these endpoints. - Peak local SAR in the exposed region reached 7.62 W/kg. Conclusion Under the specific short-term pre-clinical conditions tested, these findings indicate that 28-GHz EMR can modulate the severity of DOX-induced cardiotoxicity, while vitamin C confers modest attenuation. Further long-term and clinical studies are needed to clarify mechanisms and refine translational relevance. Importantly, this study shows that, under the specific short-term conditions, 28-GHz millimeter-wave exposure amplified several indices of doxorubicin-induced cardiac injury, whereas vitamin C provided only partial attenuation. These findings indicate a measurable interaction within this controlled co-exposure model and suggest a possible redox-mediated interaction between environmental and pharmacological stressors. These results highlight the importance of investigating potential health risks associated with electromagnetic fields such as those used in 5G technology. The conclusions of this work are restricted to a preclinical, short-duration experiment conducted in male rats without long-term follow-up. Any implications for human health remain preliminary and hypothesis-generating. Mechanistic and longitudinal studies are required to determine whether similar interactions may occur under clinically relevant exposure conditions.

AI evidence extraction

Main findings

In rats treated with doxorubicin, co-exposure to 28 GHz electromagnetic radiation amplified reductions in CAT, increased pro-apoptotic BAX expression, and prolonged the QT interval. Vitamin C partially attenuated these effects.

Outcomes measured

• Electrocardiographic parameters, including QT interval
• Serum cardiac troponin I (cTnI)
• Oxidative stress markers: MDA, GSH, SOD, and CAT
• Apoptotic and inflammatory gene expression: BAX, CASP3, BCL-2, and TNF-α
• Cardiac structural changes assessed by design-based stereology

Limitations

• Preclinical animal study
• Short-term exposure of 14 days
• Six rats per experimental group
• No group exposed to 28 GHz electromagnetic radiation without doxorubicin
• Long-term and clinical relevance was not established

{
    "study_type": "animal",
    "exposure": {
        "band": "mmWave (5G band)",
        "source": null,
        "frequency_mhz": 28000,
        "sar_wkg": null,
        "duration": "Three 10-minute cycles per day for 14 days"
    },
    "population": "Male Sprague-Dawley rats",
    "sample_size": 30,
    "outcomes": [
        "Electrocardiographic parameters, including QT interval",
        "Serum cardiac troponin I (cTnI)",
        "Oxidative stress markers: MDA, GSH, SOD, and CAT",
        "Apoptotic and inflammatory gene expression: BAX, CASP3, BCL-2, and TNF-α",
        "Cardiac structural changes assessed by design-based stereology"
    ],
    "main_findings": "In rats treated with doxorubicin, co-exposure to 28 GHz electromagnetic radiation amplified reductions in CAT, increased pro-apoptotic BAX expression, and prolonged the QT interval. Vitamin C partially attenuated these effects.",
    "effect_direction": "harm",
    "limitations": [
        "Preclinical animal study",
        "Short-term exposure of 14 days",
        "Six rats per experimental group",
        "No group exposed to 28 GHz electromagnetic radiation without doxorubicin",
        "Long-term and clinical relevance was not established"
    ],
    "evidence_strength": "low",
    "confidence": 0.979999999999999982236431605997495353221893310546875,
    "peer_reviewed_likely": "yes",
    "keywords": [
        "28 GHz",
        "5G",
        "millimeter wave",
        "electromagnetic radiation",
        "doxorubicin",
        "cardiotoxicity",
        "vitamin C",
        "oxidative stress",
        "apoptosis",
        "QT prolongation",
        "rats"
    ],
    "suggested_hubs": []
}

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