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

PAPER manual Toxicology and Applied Pharmacology 2026 Animal study Effect: harm Evidence: Low

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

At a glance
Study type
Animal study
Effect direction
harm
Population
Male Sprague-Dawley rats
Sample size
30
Exposure
mmWave 5G-band experimental exposure · 28000 MHz · 7.62 W/kg · Three 10-min cycles per day for 14 days
Evidence strength
Low
Confidence: 78% · Peer-reviewed: yes

Main findings

In a rat model of doxorubicin (DOX) cardiotoxicity, co-exposure to 28-GHz electromagnetic radiation was reported to amplify some injury-related endpoints, including greater reductions in catalase (CAT), increased pro-apoptotic BAX expression, and QT interval prolongation compared with DOX alone. Vitamin C administration provided partial protection across measured endpoints in this co-exposure model.

Outcomes measured

  • Electrocardiography (QT interval)
  • Serum cardiac troponin I (cTnI)
  • Oxidative stress markers (MDA, GSH, SOD, CAT)
  • Apoptotic gene expression (BAX, CASP3, BCL-2)
  • Inflammatory gene expression (TNF-a)
  • Cardiac structure (design-based stereology)

Limitations

  • Preclinical animal study; findings may not translate to humans
  • Short-term exposure and follow-up only (14 days)
  • Male rats only
  • Co-exposure model with doxorubicin; does not assess EMR effects in the absence of DOX beyond a sham group description
  • Mechanisms not fully established; authors call for mechanistic and longitudinal studies

Suggested hubs

  • 5g-policy (0.62)
    Study uses 28 GHz (5G-band) millimeter-wave exposure and discusses potential health risk implications.
View raw extracted JSON
{
    "publication_year": 2026,
    "study_type": "animal",
    "exposure": {
        "band": "mmWave",
        "source": "5G-band experimental exposure",
        "frequency_mhz": 28000,
        "sar_wkg": 7.62000000000000010658141036401502788066864013671875,
        "duration": "Three 10-min cycles per day for 14 days"
    },
    "population": "Male Sprague-Dawley rats",
    "sample_size": 30,
    "outcomes": [
        "Electrocardiography (QT interval)",
        "Serum cardiac troponin I (cTnI)",
        "Oxidative stress markers (MDA, GSH, SOD, CAT)",
        "Apoptotic gene expression (BAX, CASP3, BCL-2)",
        "Inflammatory gene expression (TNF-a)",
        "Cardiac structure (design-based stereology)"
    ],
    "main_findings": "In a rat model of doxorubicin (DOX) cardiotoxicity, co-exposure to 28-GHz electromagnetic radiation was reported to amplify some injury-related endpoints, including greater reductions in catalase (CAT), increased pro-apoptotic BAX expression, and QT interval prolongation compared with DOX alone. Vitamin C administration provided partial protection across measured endpoints in this co-exposure model.",
    "effect_direction": "harm",
    "limitations": [
        "Preclinical animal study; findings may not translate to humans",
        "Short-term exposure and follow-up only (14 days)",
        "Male rats only",
        "Co-exposure model with doxorubicin; does not assess EMR effects in the absence of DOX beyond a sham group description",
        "Mechanisms not fully established; authors call for mechanistic and longitudinal studies"
    ],
    "evidence_strength": "low",
    "confidence": 0.7800000000000000266453525910037569701671600341796875,
    "peer_reviewed_likely": "yes",
    "stance": "concern",
    "stance_confidence": 0.7399999999999999911182158029987476766109466552734375,
    "summary": "This animal study tested whether short-term 28 GHz (5G-band) millimeter-wave exposure modifies doxorubicin-induced cardiotoxicity in male rats and whether vitamin C mitigates effects. Co-exposure to 28 GHz EMR was reported to worsen several indices of DOX-related cardiac injury (including CAT reduction, increased BAX expression, and QT prolongation), while vitamin C provided partial attenuation. The authors emphasize that results are limited to a short-duration preclinical model and that human relevance remains preliminary.",
    "key_points": [
        "Thirty male Sprague-Dawley rats were allocated to five groups (n=6 each), including DOX-only and DOX+28 GHz EMR conditions.",
        "EMR exposure was 28 GHz for three 10-minute cycles per day over 14 days, with a reported peak local SAR of 7.62 W/kg.",
        "Doxorubicin produced functional, biochemical, molecular, and structural signs of cardiotoxicity across multiple endpoints.",
        "Co-exposure to 28 GHz EMR amplified reductions in catalase (CAT) and increased pro-apoptotic BAX gene expression compared with DOX alone.",
        "QT interval prolongation was reported in the DOX+28 GHz EMR group relative to DOX alone.",
        "Vitamin C (250 mg/kg orally for 14 days) provided partial protection across assessed endpoints in this model.",
        "The authors frame the findings as hypothesis-generating and call for longer-term and clinical studies to clarify mechanisms and relevance."
    ],
    "categories": [
        "5G/mmWave",
        "Animal Studies",
        "Cardiovascular Effects",
        "Oxidative Stress & Redox",
        "Drug–Environment Interactions"
    ],
    "tags": [
        "28 GHz",
        "5G",
        "Millimeter-Wave Exposure",
        "Specific Absorption Rate",
        "Doxorubicin Cardiotoxicity",
        "Oxidative Stress",
        "Apoptosis",
        "Catalase",
        "BAX Gene Expression",
        "QT Interval",
        "Vitamin C",
        "Rat Model",
        "Co-Exposure"
    ],
    "keywords": [
        "cardiotoxicity",
        "5G",
        "electromagnetic radiation",
        "vitamin C",
        "doxorubicin",
        "oxidative stress",
        "apoptosis"
    ],
    "suggested_hubs": [
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            "reason": "Study uses 28 GHz (5G-band) millimeter-wave exposure and discusses potential health risk implications."
        }
    ],
    "social": {
        "tweet": "Rat study: short-term 28 GHz (5G-band) exposure co-administered with doxorubicin amplified some cardiotoxicity markers (e.g., CAT reduction, BAX upregulation, QT prolongation); vitamin C offered partial attenuation. Preclinical, short-duration findings.",
        "facebook": "In a controlled rat model of doxorubicin-induced cardiotoxicity, short-term 28 GHz (5G-band) exposure was reported to worsen several cardiac injury indicators, while vitamin C provided partial protection. The authors note the results are preclinical and short-term, and human relevance remains uncertain.",
        "linkedin": "Preclinical evidence: In male rats receiving doxorubicin, co-exposure to 28 GHz (5G-band) electromagnetic radiation was reported to amplify select cardiotoxicity endpoints (oxidative/apoptotic markers and QT prolongation), with vitamin C providing partial attenuation. Authors emphasize the need for mechanistic, long-term, and clinical studies."
    }
}

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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.

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