Evidence map›Paper›PMID 41596185›Full record

ArticleAntioxidants (Basel, Switzerland)2026

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

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 and 2 more

Abstract read
In one paragraph

Article in Antioxidants (Basel, Switzerland), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

  1. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

12 authors.

Ju Hwan KimDepartment of Pharmacology, College of Medicine, Dankook University, Cheonan-si 31116, Chungnam, Republic of Korea.
Hee JinCollege of Pharmacy, Ewha Womans University, Seoul 03760, Republic of Korea.
Kyu Min JangDepartment of Pharmacology, College of Medicine, Dankook University, Cheonan-si 31116, Chungnam, Republic of Korea.
Ji Eun LeeCollege of Pharmacy, Ewha Womans University, Seoul 03760, Republic of Korea.
Sanga NaCollege of Pharmacy, Ewha Womans University, Seoul 03760, Republic of Korea.
Sangbong JeonRadio and Broadcasting Technology Laboratory, ETRI, Daejeon 34129, Republic of Korea.ORCID 0000-0001-8059-9700
Hyung-Do ChoiRadio and Broadcasting Technology Laboratory, ETRI, Daejeon 34129, Republic of Korea.ORCID 0000-0003-2652-7524
Jung Ick MoonRadio and Broadcasting Technology Laboratory, ETRI, Daejeon 34129, Republic of Korea.ORCID 0000-0001-8306-4912
Nam KimSchool of Electrical and Computer Engineering, Chungbuk National University, Cheongju 28644, Republic of Korea.ORCID 0000-0001-8109-2055
Kyung-Min LimCollege of Pharmacy, Ewha Womans University, Seoul 03760, Republic of Korea.ORCID 0000-0002-1517-7680
Hak Rim KimDepartment of Pharmacology, College of Medicine, Dankook University, Cheonan-si 31116, Chungnam, Republic of Korea.ORCID 0000-0003-3102-2272
Yun-Sil LeeCollege of Pharmacy, Ewha Womans University, Seoul 03760, Republic of Korea.ORCID 0000-0002-7538-8850

Funding

ICT R&D program of MSIT/IITP RS-2024-00466966
6 · The paper itself

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.

Indexed as

B16DNA damageHaCaTradiofrequency electromagnetic fieldsreactive oxygen speciesultraviolet

Identifiers

PMID41596185
PMCPMC12837458

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.