# 5G RF-EMFs Mitigate UV-Induced Genotoxic Stress Through Redox Balance and p38 Pathway Regulation in Skin Cells

## TL;DR

5G RF-EMFs may help reduce UV-induced DNA damage in skin cells by balancing oxidative stress and regulating the p38 pathway.

## Contribution

This study reveals a novel protective role of 5G RF-EMFs against UV-induced genotoxic stress in skin cells via redox and p38 pathways.

## Key findings

- 5G RF-EMFs reduced DNA damage markers like γH2AX and comet tail moments by 30–80%.
- RF-EMFs suppressed ROS accumulation by 56–93% and reduced p38 MAPK phosphorylation by 55–85%.
- Protective effects were comparable to N-acetylcysteine or p38 MAPK inhibitors but did not restore cell viability.

## 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.