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Journal Article
5G RF-EMFs Mitigate UV-Induced Genotoxic Stress Through Redox Balance and p38 Pathway Regulation in Skin Cells
- Authors
- Ju Hwan Kim, Hee Jin, Kyu Min Jang, Ji Eun Lee, Sanga Na, Sangbong Jeon, Hyung-Do Choi, Jung Ick Moon, Nam Kim, Kyung-Min Lim, Hak Rim Kim, Yun-Sil Lee
- Issue Date
- 2026-01
- Citation
- Antioxidants, v.15, no.1, pp.1-16
- ISSN
- 2076-3921
- Publisher
- Multidisciplinary Digital Publishing Institute (MDPI)
- Language
- English
- Type
- Journal Article
- Abstract
- The biological effects of radiofrequency electromagnetic fields (RF-EMFs) remain an unresolved scientific issue with important societal relevance, particularly in the context of the global deployment of fifth-generation (5G) wireless technologies. The skin is continuously exposed to both RF-EMFs and ultraviolet (UV) radiation, a well-established inducer of oxidative stress and DNA damage, making it a relevant model for assessing combined environmental exposures. In this study, we investigated whether post-exposure to 5G RF-EMFs (3.5 and 28 GHz) modulates ultraviolet A (UVA)-induced genotoxic stress in human keratinocytes (HaCaT) and murine melanoma (B16) cells. Post-UV RF-EMF exposure significantly reduced DNA damage markers, including phosphorylated histone H2AX (γH2AX) foci formation (by approximately 30–50%) and comet tail moments (by 60–80%), and suppressed intracellular reactive oxygen species (ROS) accumulation (by 56–93%). These effects were accompanied by selective attenuation of p38 mitogen-activated protein kinase (MAPK) phosphorylation (reduced by 55–85%). The magnitude of molecular protection was comparable to that observed with N-acetylcysteine treatment or pharmacological inhibition of p38 MAPK. In contrast, RF-EMF exposure did not reverse UV-induced reductions in cell viability or alterations in cell cycle distribution, indicating that its protective effects are confined to early molecular stress-response pathways rather than downstream survival outcomes. Together, these findings demonstrate that 5G RF-EMFs can facilitate recovery from UVA-induced molecular damage via redox-sensitive and p38-dependent mechanisms, providing mechanistic insight into the interaction between modern telecommunication frequencies and UV-induced skin stress.
- Keyword
- B16, DNA damage, HaCaT, radiofrequency electromagnetic fields, reactive oxygen species, ultraviolet
- KSP Keywords
- 28 GHz, Cell cycle distribution, Cell viability, DNA Damage, EMF Exposure, Fifth-Generation(5G), Human keratinocytes, Mitogen-activated protein kinase(MAPK), Murine melanoma, N-Acetylcysteine, Oxidative stress
This work is distributed under the term of Creative Commons License (CCL)
(CC BY)
(CC BY)
