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

Authors: Rahimi A, Rafati A, Mortazavi SMJ, Edalat F, Jooyan N, Naseh M, Keshavarz S, Jahromi HM, Nabizadeh A, Dastghaib S, Karbalaei N

Year: 2026 Feb

Category: Toxicology, Cardiology, Bioelectromagnetics

Journal: Toxicology and Applied Pharmacology

DOI: 10.1016/j.taap.2025.117703

URL: https://pubmed.ncbi.nlm.nih.gov/41478317/

Abstract

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.

cardiotoxicity 5G electromagnetic radiation vitamin C doxorubicin oxidative stress apoptosis
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