This study was performed to examine nonthermal effects of radiofrequency-field exposure on calcium dynamics in murine stem cell-derived neuronal cells.
An undifferentiated neuronal stem cell of the mouse was selected as it can be easily differentiated into neuronal cells using a known combination of biochemical factors. Furthermore some ion channels are not expressed on the stem cells in undifferentiated state until they undergo neurodifferentiation (e.g. N-type Ca2+ channel, a voltage-dependent calcium channel of the cell membrane). To elucidate the possible Ca2+ influx/efflux pathways the cells were treated with pharmacological inhibitors (amongst others nifedipine, ω-conotoxin: N-type Ca2+ channel blocker, thapsigargin: Ca2+ ATPase inhibitor).
| Frequency | 700–1,100 MHz |
|---|---|
| Type | |
| Charakteristic |
|
| Exposure duration | continuous for 60 min |
| Additional info | 700, 750, 800, 850, 900, 1000, and 1100 MHz |
| Exposure source | |
|---|---|
| Chamber | The applicator was constructed of brass with four pairs of "windows" allowing real-time optical imaging when placed on a microscope stage. An insulating well provided a buffer solution for the seeded cells. |
| Sham exposure | A sham exposure was conducted. |
| Additional info | The differentiated cells were plated on to 24 x 30 mm glass cover slips and cultured with serum-free neurobasal medium for 48 to 60 h before experiments. All experiments were conducted at room temperature of 24-26°C. |
| Measurand | Value | Type | Method | Mass | Remarks |
|---|---|---|---|---|---|
| SAR | 0.5 W/kg | - | calculated | - | - |
| Frequency | 800 MHz |
|---|---|
| Type | |
| Charakteristic |
|
| Exposure duration | continuous for 60 min |
| Exposure source |
|
|---|---|
| Sham exposure | A sham exposure was conducted. |
The exposure to radiofrequency irradiation was found to significantly increase the number of Ca2+ spikes, especially in differentiated neuronal cells (maximal number of Ca2+ spikes at a frequency of about 800 MHz). The increase in the Ca2+ spiking activities was dependent on the frequency but not on the specific absortpion rate between 0.5 to 5 W/kg. A statistical significant reduction in the number of Ca2+ spikes was observed at the 50 W/kg specific absorption rate.
No Ca2+ spikes were observed either in control cells or in the exposed cells in the absence of extracelllular Ca2+. This indicates a critical role of Ca2+ influx across the cell membrane. Using pharmacological inhibitors, it was found that both the N-type Ca2+ channels and phospholipase C enzymes appear to be involved in mediating increased Ca2+ spiking.
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