ID Number		2418
Study Type		In Vitro
Model		Study of oxidative stress in cell cultures exposed to 837 and/or 1950 MHz.
Details		AUTHORS' ABSTRACT: Hong et al. 2012 (IEEE #5760): The aim of this study was to determine whether the exposure to either single or multiple radio-frequency (RF) radiation frequencies could induce oxidative stress in cell cultures. Exposures of human MCF10A mammary epithelial cells to either a single frequency (837 MHz alone or 1950 MHz alone) or multiple frequencies (837 and 1950 MHz) were conducted at specific absorption rate (SAR) values of 4 W/kg for 2 h. During the exposure period, the temperature in the exposure chamber was maintained isothermally. Intracellular levels of reactive oxygen species (ROS), the antioxidant enzyme activity of superoxide dismutase (SOD), and the ratio of reduced/oxidized glutathione (GSH/GSSG) showed no statistically significant alterations as the result of either single or multiple RF radiation exposures. In contrast, ionizing radiation-exposed cells, used as a positive control, showed evident changes in all measured biological endpoints. These results indicate that single or multiple RF radiation exposure did not elicit oxidative stress in MCF10A cells under our exposure conditions. AUTHORS' ABSTRACT: Kang et al. 2014 (IEEE #5761):The objective of this study was to investigate the effects of the combined RF radiation (837 MHz CDMA plus 1950 MHz WCDMA) signal on levels of intracellular reactive oxygen species (ROS) in neuronal cells. Exposure of the combined RF signal was conducted at specific absorption rate values of 2 W/kg of CDMA plus 2 W/kg of WCDMA for 2 h. Co-exposure to combined RF radiation with either H2O2 or menadione was also performed. The experimental exposure groups were incubator control, sham-exposed, combined RF radiation-exposed with or without either H2O2 or menadione groups. The intracellular ROS level was measured by flow cytometry using the fluorescent probe dichlorofluorescein diacetate. Intracellular ROS levels were not consistently affected by combined RF radiation exposure alone in a time-dependent manner in U87, PC12 or SH-SY5Y cells. In neuronal cells exposed to combined RF radiation with either H2O2 or menadione, intracellular ROS levels showed no statically significant alteration compared with exposure to menadione or H2O2 alone. These findings indicate that neither combined RF radiation alone nor combined RF radiation with menadione or H2O2 influences the intracellular ROS level in neuronal cells such as U87, PC12 or SH-SY5Y. AUTHORS' ABSTRACT: Kim et al. 2016 (IEEE #6505): Purpose: To define the impact of radiofrequency (RF) under in vitro experimental Alzheimers disease conditions, we investigated the effect of RF radiation on glutamate-induced oxidative stress in mouse hippocampal neuronal HT22 cells. Materials and methods: Cell survival rate was measured by MTT and trypan blue exclusion assays. Cell cycle distribution, cell death, and ROS production were analyzed using flow cytometry. Expression of proteins was analyzed by Western blot. Results: RF exposure alone had a marginal impact on cell proliferation, however significantly enhanced glutamate-induced cytotoxicity in HT22 cells. Glutamate augmented the subG1 fraction of cell cycle, annexin/propidium iodide positive cell population, and expression of cleaved poly (ADP ribose) polymerase, which were further increased by RF exposure. Glutamate induced reactive oxygen species (ROS) generation and RF exposure further upregulated it. N-acetylcysteine (NAC) treatment completely abrogated glutamate- and RF-induced ROS production followed by cell death and restored cell proliferation in HT22 cells. Finally, glutamate phosphorylated c-Jun N-terminal kinase (JNK) and RF increased this event further. Treatment with NAC and inhibitor of JNK decreased JNK phosphorylation and restored cell proliferation, respectively. Conclusions: Our results demonstrate that RF exposure enhanced glutamate-induced cytotoxicity by further increase of ROS production in HT22 cells.
Findings		No Effects
Status		Completed With Publication
Principal Investigator		Korea Inst of Radiol and Med Sciences, Seoul, Sout
Funding Agency		?????
Country		KOREA, REPUBLIC OF
References		Hong, MN et al. Bioelectromagnetics., (2012) 33:604-611 Kang, KA et al. J Radiat Res., (2014) 55:265-276 Kim, J-Y et al. International Journal of Radiation Biology., (2017) 93:249-256 Choi, J et al. Sci Rep., (2020) 10:9238-doi: 10.1038/s41598-020-65732-4 Lee, JS et al. J. Radiat. Res., (2016) 57:620-626
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