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Ke Yao, Wei Wu, Yibo Yu, Qunli Zeng, Jiliang He, Deqiang Lu, Kaijun Wang; Effect of Superposed Electromagnetic Noise on DNA Damage of Lens Epithelial Cells Induced by Microwave Radiation. Invest. Ophthalmol. Vis. Sci. 2008;49(5):2009-2015. doi: https://doi.org/10.1167/iovs.07-1333.
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purpose. To investigate the influence of the 1.8-GHz radiofrequency fields (RFs) of the Global System for Mobile Communications on DNA damage, intracellular reactive oxygen species (ROS) formation, cell cycle, and apoptosis in human lens epithelial cells (hLECs) and whether the effects induced by RF could be blocked by superposing of electromagnetic noise.
methods. After 24-hour intermittent exposure at the specific absorption rate of 1 W/kg, 2 W/kg, 3 W/kg, and 4 W/kg, the DNA damage of hLECs was examined by alkaline comet assay and immunofluorescence microscope detection of the phosphorylated form of histone variant H2AX (γH2AX) foci, respectively. ROS production was quantified by the fluorescent probe 2′,7′-dichlorodihydrofluorescein diacetate (DCFH-DA). Cell cycle and cell apoptosis were determined by flow cytometry.
results. DNA damage examined by alkaline comet assay was significantly increased after 3 W/kg and 4 W/kg radiation (P < 0.05), whereas the double-strand breaks (DSBs) evaluated by γH2AX foci were significantly increased only after 4 W/kg radiation (P < 0.05). Significantly elevated intracellular ROS levels were also detected in the 3-W/kg and 4-W/kg groups (P < 0.05). After exposure to 4 W/kg for 24 hours, hLECs exhibited significant G0/G1 arrest (P < 0.05). There was no detectable difference in cell apoptosis between the microwave radiation and sham exposure groups (P > 0.05). All the effects mentioned were blocked when the RF was superposed with 2 μT electromagnetic noise.
conclusions. Microwave radiation induced hLEC DNA damage after G0/G1 arrest does not lead to cell apoptosis. The increased ROS observed may be associated with DNA damage. Superposed electromagnetic noise blocks microwave radiation-induced DNA damage, ROS formation, and cell cycle arrest.
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