この研究は、マウス胎児幹細胞株から分化した神経細胞に対する700－1100 MHz無線周波（RF）電磁界の非熱的な影響として、Caイオンスパイク（Caイオン流入により発生する活動電位）およびCaイオン動態の変化を調べた。その結果、無ばく露の対照群では、60％の細胞において60分間に1細胞当たり5回の自発的スパイクが観察されたのに対し、ばく露群（800 MHz、0.5 W/kg）ではスパイクが15.7±0.8回と有意に増加した；スパイク頻度の増加は周波数に依存し、SAR（0.5－5 W/kg）には依らなかった；薬物を利用した実験で、N型CaイオンチャネルとホスフォリパーゼC酵素がこのスパイク増加に介在することが示された、などを報告している。
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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).
|ばく露時間||continuous for 60 min|
|Additional information||700, 750, 800, 850, 900, 1000, and 1100 MHz|
|チャンバの詳細||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 information||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.|
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.