Zhijian, C.; Xiaoxue, L.; Yezhen, L.; Deqiang, L.; Shijie, C.; Lifen, J.; Jianlin, L., and Jiliang, H. Influence of 1.8-GHz (GSM) radiofrequency radiation (RFR) on DNA damage and repair induced by X-rays in human leukocytes in vitro. Mutat Res. 2009 Jun-2009 Jul 31; 677(1-2):100-4.
As most studies have demonstrated that RF radiation (RFR) at non-thermal densities do not directly induce DNA damage, the general consensus is that RFR is not directly genotoxic. Therefore, the importance of research into its possible indirect effects and synergic effects on DNA damage with other environmental agents has been highlighted. The results of research in this area are, however, controversial and inconclusive. In the authors’ previous experiments, synergic effects on DNA damage induced in human leukocytes by some chemical mutagens, a physical factor ultraviolet radiation, and 1.8 GHz non-thermal RFR were observed. The combined effect of RFR and X-rays on DNA damage was previously studied by other investigators. However, the influence of non-thermal RFR on the repair of X-ray-induced DNA damage has not been studied.
The aim of this study was to examine in vitro the synergic effect of non-thermal 1.8 GHz RFR and X-rays on DNA damage in human leukocytes and the impact of non-thermal RFR radiation on the kinetic of repair of DNA damage induced by different doses of X-rays.
Blood samples were obtained from four non-smoking healthy donors. The leukocytes were exposed to the 1.8 GHz RFR signal, simulating the GSM signal, for 24 hours (field on for 5 min, field off for 10 min) at SAR of 2W/kg. After RF exposure or sham exposure, the leukocytes were exposed to X-rays at doses 0.25, 0.5, 1.0 and 2.0 Gy. DNA damage was detected by comet assay at 0, 15, 45, 90, 150 and 240 min after the X-ray exposure. The percent of DNA in the tail was used as the indicator of DNA damage, and the DNA repair percentage - as the indicator of the DNA repair speed.
There was no significant difference in the leukocyte DNA damage between the RFR exposed and the sham exposed group (P>0.05). There was a significant dose-effect relationship between the X-ray dose and DNA damage (p<0.05) and a variation among the four donors. No significant difference in the X-ray-induced DNA damage was observed between the RFR exposed and the sham exposed groups (P>0.05). There were individual differences among the four donors in the DNA repair speed after X-ray exposure. Only in two cases (donor 3, X-ray dose 1.0 Gy and donor 4, X-ray dose 0.25 Gy) there was a significant difference between the RFR exposed and the sham exposed groups in the speed of repair of X-ray induced DNA damage.
Interpretation and conclusion
The exposure to 1.8 GHz RFR at 2 W/kg for 24 hours did not directly induce DNA damage and did not influence the X-ray induced DNA damage. These results are consistent with the results of other investigators. In most cases, the RFR exposure had no impact on the kinetic of DNA repair in the X-ray exposed leukocytes. The two cases with a suggestion of the influence of the RFR exposure on repair of the X-ray induced DNA damage may be explained by individual leukocyte’s responses to RFR.