Luukkonen J, Hakulinen P, Mäki-Paakkanen J, Juutilainen J, Naarala J. Enhancement of chemically induced reactive oxygen species production and DNA damage in human SH-SY5Y neuroblastoma cells by 872 MHz radiofrequency radiation. Mutat Res 24 Dec 2008 Ahead of print.
One of the major concerns related to the rapidly increasing use of mobile phones is possible genotoxicity of radiofrequency (RF) radiation emitted by these devices. Most studies have not found any genotoxic effect at specific absorption rates (SARs) below 2 W/kg, i.e. at the levels typically associated with mobile phone use. The evidence is more inconclusive at high SAR values (>2 W/kg). Because of the low photon energy of RF radiation, it is not considered to induce direct alterations in DNA. One of the mechanisms leading to DNA damage, cellular oxidative stress that results from an increase in intracellular reactive oxygen species (ROS), has not been widely investigated in relation to possible causation by RF radiation. Another interesting question is whether RF radiation is able to enhance the mutagenic properties of known mutagens. If RF radiation enhances ROS-generating effects of other agents, such effect could lead to enhancement of their other effects, such as genotoxicity and carcinogenicity.
The aim of the study was to investigate whether RF radiation at a relatively high SAR induces cellular ROS production or alters the effects of a ROS-generating chemical agent (menadione), and whether the possible RF radiation-related ROS changes are linked to DNA damage. In addition, the effects of GSM modulated RF radiation were compared with those of the continuous wave (CW) RF radiation.
Human SH-SY5Y neuroblastoma cells were exposed in four groups: 1) sham-exposed control; 2) RF radiation; 3) menadione, and 4) RF radiation + menadione. The exposures to 872 MHz CW or GSM modulated (pulsed at 217 pulses per second) RF radiation were conducted at SAR of 5 W/kg. Exposure time for each experiment was 1 hour. Cell viability was determined by adding propidium iodide, a fluorescent probe that binds to chromatin on loss of membrane integrity. The production of ROS was measured using the fluorescent probe dichlorofluorescein, and DNA damage was evaluated by the alkaline Comet assay.
In menadione and CW RF exposed cells, ROS production was significantly higher than in cells exposed to menadione only at time points 30 minutes (P<0.05) and 60 minutes (P<0.01) after the end of exposure. No effects of the GSM signal were seen on ROS production. Addition of menadione decreased cell viability significantly (p≤0.001). RF radiation did not affect cell viability significantly. Exposure to menadione resulted in a significantly (p≤0.001) increased DNA damage. A further enhancement was observed in the menadione+CW radiation exposed group compared to the menadione only exposed group (p<0.01). No genotoxic effect was observed from CW RF radiation alone. GSM modulated RF radiation did not induce DNA damage alone or in combination with menadione.
The results of the study suggest that CW RF radiation but not GSM modulated RF radiation might enhance chemically induced effects, namely ROS production and DNA damage. Some studies have reported an effect of RF radiation, in particular CW radiation, on ROS production, while others have not shown any effects on cellular ROS levels, with or without different combined exposures. To the author’s knowledge, the present study has investigated effects of RF radiation on intracellular ROS production using the highest SAR level so far, which highlights the importance for reproducibility studies. The finding that RF radiation does not affect cell viability is consistent with other studies. The enhancement of chemically induced DNA damage observed in this study was associated with CW RF radiation but not with the GSM signal. As is often the case with the literature on biological effects of RF radiation, contradictory results are reported, and different RF signals, cell types and SAR levels complicate comparison between studies.
The increased DNA damage and enhanced ROS production observed in this study may be causally related. The internal consistency of the findings (both alterations were associated only with CW RF) might be interpreted to support causality. However, there is no known or hypothetical mechanism for effects from a CW signal but not from a pulse-modulated signal at identical SAR level.
The results of the present study suggest that 872 MHz CW RF radiation at 5 W/kg might enhance chemically induced ROS production and thus cause secondary DNA damage. However, there is no known mechanism that would explain such effect from CW RF radiation but not from GSM modulated RF radiation at identical SAR.