The authors systematically investigated the effects of radiofrequency electromagnetic fields on DNA damage by examining and comparing gamma-H2AX foci formation in six cell types after GSM 1800 MHz exposure. Since the gamma-H2AX foci formation is an early marker of DNA damage, it was also investigated whether the exposure-induced gamma-H2AX foci formation resulted in genetic instabilities, aberrant cell cycle progression and other cellular dysfunctions.
Positive controls were performed with 4-nitroquinoline 1-oxide. All experiments were repeated a number of times.
|Setup||two waveguides, one for RF and one for sham exposure; six 35-mm Petri dishes were placed in the H-field maximum of the standing wave|
|Sham exposure||A sham exposure was conducted.|
|Additional info||the temperature of the system remained at 37 ± 0.1°C during the whole exposure duration, and the temperature difference between radiofrequency and sham exposed cultures never exceeded 0.1°C.|
Exposure to radiofrequency electromagnetic fields for 24 h significantly induced gamma-H2AX foci formation in CHL cells and human skin fibroblasts, but not in the other cell types. However, exposure-elevated gamma-H2AX foci formation in human skin fibroblasts did not result in detectable DNA fragmentation, sustainable cell cycle arrest (slightly increased G0 phase/G1 phase arrest at 6 h after exposure but not at 12 h), cell proliferation or cell viability change. Radiofrequency electromagnetic field exposure slightly but not significantly increased the cellular reactive oxygen species level.
In conclusion, the radiofrequency exposure induced a DNA damage in a cell type-dependent manner, but the elevated gamma-H2AX foci formation in human skin fibroblasts did not result in significant cellular dysfunctions. The observed DNA damage might be reversible or compensated by DNA repair pathways or other cellular processes under the current experimental conditions.