ID Number		2288
Study Type		In Vitro
Model		In vitro study of DNA damage in cells exposed to 1800 MHz.
Details		AUTHORS' ABSTRACT: Xu et al. 2013 (IEEE #5228): BACKGROUND: Although IARC clarifies radiofrequency electromagnetic fields (RF-EMF) as possible human carcinogen, the debate on its health impact continues due to the inconsistent results. Genotoxic effect has been considered as a golden standard to determine if an environmental factor is a carcinogen, but the currently available data for RF-EMF remain controversial. As an environmental stimulus, the effect of RF-EMF on cellular DNA may be subtle. Therefore, more sensitive method and systematic research strategy are warranted to evaluate its genotoxicity. OBJECTIVES: To determine whether RF-EMF does induce DNA damage and if the effect is cell-type dependent by adopting a more sensitive method ³H2AX foci formation; and to investigate the biological consequences if RF-EMF does increase ³H2AX foci formation. AUTHORS' ABSTRACT: Su et al. 2016 (IEEE #6582): Despite many years of studies, the debate on genotoxic effects of radiofrequency electromagnetic fields (RF-EMF) continues. To systematically evaluate genotoxicity of RF-EMF, this study examined effects of RF-EMF on DNA damage and cellular behavior in different neurogenic cells. Neurogenic A172, U251, and SH-SY5Y cells were intermittently (5 min on/10 min off) exposed to 1800 MHz RF-EMF at an average specific absorption rate (SAR) of 4.0 W/kg for 1, 6, or 24 h. DNA damage was evaluated by quantification of ³H2AX foci, an early marker of DNA double-strand breaks. Cell cycle progression, cell proliferation, and cell viability were examined by flow cytometry, hemocytometer, and cell counting kit-8 assay, respectively. Results showed that exposure to RF-EMF at an SAR of 4.0 W/kg neither significantly induced ³H2AX foci formation in A172, U251, or SH-SY5Y cells, nor resulted in abnormal cell cycle progression, cell proliferation, or cell viability. Furthermore, prolonged incubation of these cells for up to 48 h after exposure did not significantly affect cellular behavior. Our data suggest that 1800 MHz RF-EMF exposure at 4.0 W/kg is unlikely to elicit DNA damage or abnormal cellular behaviors in neurogenic cells. METHODS: Six different types of cells were intermittently exposed to GSM 1800 MHz RF-EMF at a specific absorption rate of 3.0 W/kg for 1 h or 24 h, then subjected to immunostaining with anti-³H2AX antibody. The biological consequences in ³H2AX-elevated cell type were further explored with comet and TUNEL assays, flow cytometry, and cell growth assay. RESULTS: Exposure to RF-EMF for 24 h significantly induced ³H2AX foci formation in Chinese hamster lung cells and Human skin fibroblasts (HSFs), but not the other cells. However, RF-EMF-elevated ³H2AX foci formation in HSF cells did not result in detectable DNA fragmentation, sustainable cell cycle arrest, cell proliferation or viability change. RF-EMF exposure slightly but not significantly increased the cellular ROS level. CONCLUSIONS: RF-EMF induces DNA damage in a cell type-dependent manner, but the elevated ³H2AX foci formation in HSF cells does not result in significant cellular dysfunctions. AUTHORS' ABSTRACT: Sun et al. 2016 (IEEE #6569): Radiofrequency electromagnetic fields (RF-EMFs) have been classified by the International Agency for Research on Cancer as possible carcinogens to humans; however, this conclusion is based on limited epidemiological findings and lacks solid support from experimental studies. In particular, there are no consistent data regarding the genotoxicity of RF-EMFs. Ataxia telangiectasia mutated (ATM) is recognised as a chief guardian of genomic stability. To address the debate on whether RF-EMFs are genotoxic, we compared the effects of 1,800 MHz RF-EMF exposure on genomic DNA in mouse embryonic fibroblasts (MEFs) with proficient (Atm+/+) or deficient (Atm-/-) ATM. In Atm+/+ MEFs, RF-EMF exposure for 1 h at an average special absorption rate of 4.0 W/kg induced significant DNA single-strand breaks (SSBs) and activated the SSB repair mechanism. This effect reduced the DNA damage to less than that of the background level after 36 hours of exposure. In the Atm-/- MEFs, the same RF-EMF exposure for 12 h induced both SSBs and double-strand breaks and activated the two repair processes, which also reduced the DNA damage to less than the control level after prolonged exposure. The observed phenomenon is similar to the hormesis of a toxic substance at a low dose. To the best of our knowledge, this study is the first to report a hormesis-like effect of an RF-EMF. AUTHORS' ABSTRACT: Su et al. 2018 (IEEE #6989): PURPOSE: To systematically evaluate the effects of 1800 MHz radiofrequency electromagnetic fields (RF-EMF) exposure on DNA damage and cellular functions in primary cultured neurogenic cells. MATERIALS AND METHODS: The primary cultured astrocytes, microglia and cortical neurons were exposed to RF-EMF at a SAR of 4.0 W/kg. The DNA damage was evaluated by ³H2AX foci formation assay. The secretions of pro-inflammatory cytokines (TNF-±, IL-6 and IL-1²) in astrocytes and microglia, microglial phagocytic activity and neuronal development were examined by enzyme-linked immunosorbent assay, phagocytosis assay and immunofluorescent staining on microtubule-associated protein tau, microtubule-associated protein 2, postsynaptic density 95 and gephyrin, respectively. RESULTS: RF-EMF exposure did not significantly induce ³H2AX foci formation in three primary cultured neurogenic cells. Furthermore, RF-EMF exposure did not significantly affect the secretion of cytokines in astrocytes and microglia, and the morphological indicators of dendrites or synapses of cortical neurons. However, the exposure significantly reduced the phagocytic activity of microglia and inhibited the axon branch length and branch number of cortical neurons. CONCLUSIONS: Our data demonstrated that exposure to RF-EMF did not elicit DNA damage but inhibited the phagocytic ability of microglia and the axon branch length and branch number of cortical neurons.
Findings		Effects
Status		Completed With Publication
Principal Investigator		Zhejiang U Sch of Medicine, Hangzhou
Funding Agency		?????
Country		CHINA
References		Xu, S et al. PLoS One., (2013) 8:(10 pages)-doi: 10.1371/journal.pone.0054906 Sun, C et al. Sci Rep., (2016) 6:37423- Su, L et al. Bioelectromagnetics., (2017) 38:175-185 Su, L et al. Int J Radiat Biol. , (2018) 94:295-305
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