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The Protective Effects of EMF-LTE against DNA Double-Strand Break Damage In Vitro and In Vivo.
Jin, Hee; Kim, Kyuri; Park, Ga-Young; Kim, Minjeong; Lee, Hae-June; Jeon, Sangbong; Kim, Ju Hwan; Kim, Hak Rim; Lim, Kyung-Min; Lee, Yun-Sil.
Afiliação
  • Jin H; College of Pharmacy, Ewha Womans University, Seoul 03760, Korea.
  • Kim K; College of Pharmacy, Ewha Womans University, Seoul 03760, Korea.
  • Park GY; College of Pharmacy, Ewha Womans University, Seoul 03760, Korea.
  • Kim M; College of Pharmacy, Ewha Womans University, Seoul 03760, Korea.
  • Lee HJ; Division of Basic Radiation Bioscience, Korea Institute of Radiological & Medical Sciences, Seoul 03760, Korea.
  • Jeon S; Radio & Satellite Research Division, Electronics and Telecommunications Research Institute, Daejeon 34129, Korea.
  • Kim JH; Department of Pharmacology, College of Medicine, Dankook University, Chungnam 31116, Korea.
  • Kim HR; Department of Pharmacology, College of Medicine, Dankook University, Chungnam 31116, Korea.
  • Lim KM; College of Pharmacy, Ewha Womans University, Seoul 03760, Korea.
  • Lee YS; College of Pharmacy, Ewha Womans University, Seoul 03760, Korea.
Int J Mol Sci ; 22(10)2021 May 12.
Article em En | MEDLINE | ID: mdl-34066270
With the rapid growth of the wireless communication industry, humans are extensively exposed to electromagnetic fields (EMF) comprised of radiofrequency (RF). The skin is considered the primary target of EMFs given its outermost location. Recent evidence suggests that extremely low frequency (ELF)-EMF can improve the efficacy of DNA repair in human cell-lines. However, the effects of EMF-RF on DNA damage remain unknown. Here, we investigated the impact of EMF-long term evolution (LTE, 1.762 GHz, 8 W/kg) irradiation on DNA double-strand break (DSB) using the murine melanoma cell line B16 and the human keratinocyte cell line HaCaT. EMF-LTE exposure alone did not affect cell viability or induce apoptosis or necrosis. In addition, DNA DSB damage, as determined by the neutral comet assay, was not induced by EMF-LTE irradiation. Of note, EMF-LTE exposure can attenuate the DNA DSB damage induced by physical and chemical DNA damaging agents (such as ionizing radiation (IR, 10 Gy) in HaCaT and B16 cells and bleomycin (BLM, 3 µM) in HaCaT cells and a human melanoma cell line MNT-1), suggesting that EMF-LTE promotes the repair of DNA DSB damage. The protective effect of EMF-LTE against DNA damage was further confirmed by attenuation of the DNA damage marker γ-H2AX after exposure to EMF-LTE in HaCaT and B16 cells. Most importantly, irradiation of EMF-LTE (1.76 GHz, 6 W/kg, 8 h/day) on mice in vivo for 4 weeks reduced the γ-H2AX level in the skin tissue, further supporting the protective effects of EMF-LTE against DNA DSB damage. Furthermore, p53, the master tumor-suppressor gene, was commonly upregulated by EMF-LTE irradiation in B16 and HaCaT cells. This finding suggests that p53 plays a role in the protective effect of EMF-LTE against DNA DSBs. Collectively, these results demonstrated that EMF-LTE might have a protective effect against DNA DSB damage in the skin, although further studies are necessary to understand its impact on human health.
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Texto completo: 1 Base de dados: MEDLINE Assunto principal: Radiação Ionizante / Ondas de Rádio / Queratinócitos / Substâncias Protetoras / Campos Eletromagnéticos / Quebras de DNA de Cadeia Dupla / Melanoma Idioma: En Ano de publicação: 2021 Tipo de documento: Article

Texto completo: 1 Base de dados: MEDLINE Assunto principal: Radiação Ionizante / Ondas de Rádio / Queratinócitos / Substâncias Protetoras / Campos Eletromagnéticos / Quebras de DNA de Cadeia Dupla / Melanoma Idioma: En Ano de publicação: 2021 Tipo de documento: Article