この研究は、ペンチレンテトラゾール（PTZ）投与により作成したラットのてんかん動物モデルの海馬および後根神経節（DRG）における、（TRPV1チャネルを経た）カルシウムイオン流入、酸化ストレス、アポトーシスに対するWi-Fi（2.45 GHz）ばく露の影響を調べた。ラットを、対照群、PTZ + Wi-Fi群、PTZ + Wi-Fi + カプサゼピン（CPZ：TRPV1阻害薬） に分けた。Wi-Fiの1時間ばく露の後にカプサイシン（CAP）刺激を行い、海馬、DRGのニューロンを単離して検査した。その結果、PTZ群では、対照群に比べ、海馬の細胞質遊離カルシウムイオン、活性酸素種、アポトーシス、ミトコンドリア膜脱分極などが高くなり、一方、細胞生存率は低下した；Wi-Fiばく露により、細胞質遊離カルシウム上昇の影響はさらに大きくなった；しかし、CPZ投与群では、てんかん誘導性のカルシウムイオン流入、酸化ストレス、アポトーシスは防止された、と報告している。
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The effects of exposure of hippocampal and dorsal root ganglion neurons of rats to a 2.45 GHz electromagnetic field (WLAN) on TRPV1 ion channel activity, oxidative stress and apoptosis in association with epilepsy should be investigated.
In the study, two different types of cells were extracted from rats and divided into the following groups: a) groups using hippocampal neurons: 1) from healthy rats (n=10) (control group), 2) from epileptic rats (n=8 or 10?), 3) exposed neurons from epileptic rats (n=8 or 10?), 4) exposed neurons from epileptic rats (n=8 or 10?) and addition of capsazepine.
b) groups using dorsal root ganglion neurons: 5) from healthy rats (n=8) (control group), 6) treatment with capsaicin (from 6 rats), 7) exposed neurons (from 6 rats), 8) exposed neurons (from 6 rats) and addition of capsaicin plus capsazepine after 1 hour, 9) treatment with different calcium channel inhibitors (from 6 rats), 10) exposed neurons and treatment with different calcium channel inhibitors (from 6 rats).
TRPV1 is a calcium-permeable and non-selective ion channel, gated by noxious heat, oxidative stress and capsaicin. To induce epilepsy, pentylenetetrazol was administered to rats. Capsaicin was used to activate TRPV1 ion channels while capsazepine was used as a capsaicin antagonist to block TRPV1.
|ばく露時間||continuous for 1 hour|
|Repetition frequency||217 Hz|
remark EMF-Portal: The authors also mention a continuous wave (?).
|Distance between exposed object and exposure source||25 cm|
|チャンバの詳細||exposure system was kept in a specific room which included plastic furniture and the walls of the room were covered by chromium-nickel plates (diameter: 1 mm) for shielding against environmental EMF|
|ばく露装置の詳細||cells were kept in 15 ml Falcon tubes placed in a non-conductive plexi glass table in a circulatory water bath next to the antenna; temperature in room and in tubes was maintained at 37°C (relative humidity of 83 %)|
The free intracellular calcium, oxidative stress, apoptosis, mitochondrial membrane depolarization and the enzyme activities of caspase-3 and -9 were significantly increased while cell viability was significantly decreased in epileptic rat hippocampus neurons (group 2) compared to the control group. Additional WLAN exposure (group 3) induced a further intracellular calcium increase, while a treatment of the neurons with capsazepine (group 4) resulted in a protection against epilepsy-induced calcium influx, apoptosis and oxidative stress.
The test on TRPV1 ion channel activity in WLAN exposed and non-exposed dorsal root ganglion neurons and treatment with calcium channel inhibitors (group 10) indicated that WLAN exposure induced calcium influx via the TRPV1 channels.
The authors conclude that exposure of hippocampal and dorsal root ganglion neurons of rats to a 2.45 GHz electromagnetic field (WLAN) and epilepsy could induce a calcium influx in cells via TRPV1 ion channels, oxidative stress and apoptosis and that capsazepine might attenuate these effects.