この実験研究は、ラットの脳および後根神経節（DRG）のニューロンにおける抗酸化還元システム、Ca2+流入、細胞バイアビリティ、脳電図（EEG）記録に対する2.45GHz電磁界（EMR）ばく露の影響とそれに対するメラトニンの保護効果を調べた。32匹のWistarアルビノ雄ラットを無作為に4群（各8匹。A1：ケージ対照群、A2：擬似ばく露群、B：EMR群、C：EMR+メラトニン群）に分けた。EMR群は、60分/日で30 日間ばく露。ばく露装置は、モノポールアンテナの周囲に8匹のラットの頭部を中心に向けて放射状に固定して並べたもの（頭とアンテナの距離1cm、SARは約0.14W/kgと計算した）。C群は、B群と同じEMRばく露の他に、腹腔内注射によりメラトニン10 mg/kg/日を投与した。実験終了後、各群についてEEG測定した後、屠殺して脳とDRGの標本を採取した。その結果、DRGニューロンの脂質過酸化、細胞バイアビリティ、細胞内Ca2+レベルはA1、A2群よりB群の方が高かった；EEGのスパイク数はB群よりC群の方が少なかった；皮質のビタミンE濃度はB群よりC群の方が高かったなどの所見を報告している。
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To investigate the effects of a 2.45 GHz electromagnetic field exposure on the brain cortex and the dorsal root ganglion of rats, as well as the possible protective effects of melatonin administration.
4 groups (n=8 per group) were examined: 1.) cage control, 2.) sham exposure + daily injection of saline, 3.) exposure and 4.) exposure + daily injection of melatonin (10 mg/kg).
Before the animals were killed, an EEG was recorded. Afterwards, brain homogenates and the dorsal root ganglion were investigated for signs of oxidative stress. Additionally, in the dorsal root ganglion, the intracellular calcium concentration was determined and the patch-clamp technique was conducted.
|ばく露時間||continuous for 1 h/day on 30 days|
|Repetition frequency||217 Hz|
|Distance between exposed object and exposure source||1 m|
|ばく露装置の詳細||rats kept in 15 cm long cylindrical constrainers with a diameter of 5 cm; 8 constrainers positioned radially on a groundplate with the antenna in the center; rats placed with their heads near the antenna|
|Sham exposure||A sham exposure was conducted.|
In general, no differences were found between the cage control (group 1) and the sham exposed group (group 2).
In the exposed group (group 3), the number of spikes in the EEG was increased compared to the control groups (group 1+2). However, no differences occurred in the EEG between the exposed group treated with melatonin (group 4) and the control groups (groups 1+2).
In the dorsal root ganglia of exposed rats (group 3), the cell viability was significantly decreased compared to the control groups (group 1+2). In contrast, there was no difference in the cell viability between the melatonin treated exposure group (group 4) and the control groups (groups 1+2). Additionally, in the exposed group (group 3), the level of lipid peroxidation and the intracellular calcium release were increased in comparison to the control groups (groups 1+2). Again, no differences in the level of lipid peroxidation and the intracellular calcium release were found between the melatonin treated exposure group (group 4) and the control groups (group 1+2). The current densities of the neurons were higher in the exposed group (group 3) than in the control groups (groups 1+2).
In brain homogenates of exposed rats, treated with melatonin (group 4), an increased concentration of vitamin E was found, whereas the concentration of vitamin E in the other groups (groups 1+2+3) did not change.
Remaining brain homogenate and dorsal root ganglion antioxidant values were not affected by exposure or melatonin administration.
The authors conclude that exposure to a wireless device of 2.45 GHz could induce oxidative stress in the dorsal root ganglion and that melatonin could prevent such a reaction.