engleski

Cellular response to short-term 1800 MHz radiofrequency radiation exposure

Objective Rapid progress in the field of telecommunications has raised concern about possible hazardous effect of radiofrequency (RF) radiation on living organism. Although potential health impacts of RF exposure have been extensively studied, there are many uncertainties and questions regarding biological effects that occur at the non-thermal level. One of the important mechanisms that should be considered is connected to redox imbalance and development of oxidative stress. The aim of this study was to measure and compare the biological effect of short-term 1800 MHz RF exposure on two morphological and functional distinct cell culture types. Methods Chinese hamster lung fibroblast cells (V79) and human neuroblastoma cells (SH-SY5Y) were exposed to 1800 MHz modulated RF radiation at field strength of 30 V/m. The cell samples were irradiated inside of the Gigahertz Transverse Electromagnetic Cell (GTEM) for 10, 30 and 60 minutes. Cellular viability was measured by 3-(4, 5-dimethylthiazole-2-yl)-2, 5-diphenyltetrazolium bromide assay (MTT) and level of reactive oxygen species (ROS) was determined by fluorescent probe 2′, 7′-dichlorofluorescein diacetate (DCFH-DA). Enzyme-linked immunosorbent assay (ELISA) was used to measure concentrations of oxidised proteins and malondialdehyde (MDA) was used to assess the level of lipid oxidative damage. Results Average specific absorption rate (SAR) was calculated to be 1.6 W/kg. The viability of radiation exposed cells remained within normal physiological values throughout the measurement period. In V79 cells 10-minute radiation caused significant increase in the level of ROS, while higher ROS values in SH-SY5Y cells were observed for every radiation exposure time. After 60-minute exposure there was significant protein and lipid oxidative damage in SH-SY5Y cells. Conclusion Modulated radiofrequency radiation at non-thermal level induces disbalance of cellular redox equilibrium. Applied radiation caused transient changes in V79 cells, suggesting activation of adaptation mechanisms, while due to its neural origin, SH-SY5Y cells appeared to be more sensitive to radiation exposure.

cell viability ; lipid damage ; oxidised proteins ; reactive oxygen species

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