Autores

Belyaev I, Markova E, Malmgren L. Microwaves from Mobile Phones Inhibit 53BP1 Focus Formation in Human Stem Cells Stronger than in Differentiated Cells: Possible Mechanistic Link to Cancer Risk. Environ Health Perspect. Oct 22, 2009 Ahead of print.

Background
Stem cells have been considered as a target for origination of cancer. DNA double-strand breaks (DSB) and their misrepair are critical molecular events leading to chromosome aberrations (CA), which have been associated with various tumours. Several proteins involved in double-strand breaks repair, such as the tumor suppressor T53 binding protein 1 (53BP1) produce foci at the sites of double-strand breaks location. Inability to form DNA repair foci has been associated with various DNA repair defects, and inhibition of double-strand breaks repair may lead to chromosome aberrations. In their previous studies, the authors have shown that microwave exposure inhibited formation of endogenous DNA repair foci in human lymphocytes. They believe that, if similar effects can be detected in microwave exposed stem cells, this may provide a mechanistic explanation of epidemiological data showing association between microwave exposure and increased cancer risk.

Objective
The objective of the study was to investigate whether microwaves from GSM and UMTS mobile phones induce double-strand breaks or affect double-strand break repair in human stem cells and to compare the response of stem cells with the response of differentiated human cells (fibroblasts).

Methods
Mesenchymal stem cells (MSC) from adipose tissue of 2 healthy individuals and diploid VH-10 fibroblasts from the foreskin of a healthy boy were used in this study. The cells were exposed to either GSM (905 MHz or 915 MHz (SAR=37 mW/kg)) or UMTS (1947.4 MHz (SAR=39 mW/kg)). Temperature measurements were conducted before, during and after exposure, and no temperature changes were detected. Sham-exposed cells were used as controls. The heat treatment (41°C) was used as a positive control for stress response, and exposure to 137Cs g-rays at the dose of 3 Gy and dose rate of 10.6 Gy/min – as a positive control for genotoxic effect. 53BP1 foci were analyzed by laser confocal microscopy.

Results
Irradiation with gamma-rays at 3 Gy resulted in a significant increase in 53BP1 foci both in fibroblasts and in mesenchymal stem cells. A significant reduction in the level of these foci was observed in fibroblasts after exposure to 915 MHz GSM (p<0.003) and to UMTS microwaves (p<0.01) regardless of the duration of exposure within 1-3 hours, and after heat treatment (p<0.001). Exposure to 905 MHz GSM did not affect fibroblasts. There was a significant difference between the effects of 915 MHz and 905 MHz microwaves in fibroblasts (p<0.01). Similar to fibroblasts, a distinct reduction in the level of endogenous 53BP1 foci was observed in mesenchymal stem cells exposed to 915 MHz GSM and UMTS microwaves (p<0.0005) regardless of exposure duration, and in mesenchymal stem cells exposed to heat. These effects in mesenchymal stem cells were more pronounced than in fibroblasts. In contrast to fibroblasts, approximately 5% of mesenchymal stem cells had multiple foci (more than 10 foci/cell), which were inhibited by microwave exposure. Some (non- significant) reduction in foci formation was observed in mesenchymal stem cells after exposure to 905 MHz GSM. In contrast to fibroblasts, there was no significant difference between the effects of 905 MHz and 915 MHz exposures. In experiments with chronic exposure (5 days per week, 1 hour daily) it was shown that fibroblasts almost completely adapted to the chronic exposure, but no such adaptation was seen in stem cells.

Interpretation
For the first time, it has been reported that exposure of human mesenchymal stem cells and primary fibroblasts to microwave from GSM/UMTS mobile phones inhibit formation of endogenous 53BP1 foci. Similar effect was previously observed by the authors in human lymphocytes. Since the SAR values were below the thermal level and no changes in temperature in the exposed samples were observed, these effects could not be attributed to heating. While fibroblasts adapt to the exposure, no such adaptation was observed in stem cells. The results indicate that human stem cells are more sensitive to microwave exposure than differentiated primary cells. As no increase in effect was observed in either fibroblasts or mesenchymal stem cells at prolongation of exposure up to 3 hours (compared to 1 hour), saturation of the effect can be suggested. The effects of microwave exposure are dependent on carrier frequency. Stem cells may react to more frequencies than differentiated primary human cells.

Conclusion
The authors concluded that their results “may be important for cancer risk assessment and indicate that stem cells are most relevant cellular model for validating the safe mobile communication signals.”



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