ミトコンドリアDNA（mtDNA）欠損とさまざまな神経系疾患との間には密接な関係があり、またmtDNAは酸化ストレスに極めて弱いことに着目して、この実験研究ではRF電磁界によるmtDNAの酸化的損傷（一般的バイオマーカーは8-ヒドロキシグアニン（8-OHdG）を指標として）を評価した。用いた細胞は初代培養皮質ニューロン、ばく露は217 Hzでパルス変調した1800 MHz電磁界、SAR＝2 W/kg、ばく露時間24時間とした。その結果、8-OHdGの有意な濃度上昇、mtDNAのコピー数とミトコンドリアRNA転写産物のレベルの顕著な減少が見られたと報告している。
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To study whether radiofrequency irradiation can cause oxidative damage to mitochondrial DNA (mtDNA) in primary cultured cortical neurons of rats.
mtDNA defects are closely associated with various nervous system diseases and mtDNA is particularly susceptible to oxidative stress.
The cells were assigned to one of five groups: (1) sham exposure group, (2) melatonin group, (3) radiofrequency exposure group, (4) radiofrequency exposure+melatonin group, (5) hydrogen peroxide exposure (100 µM for 24 h, as a positive control of oxidative stress). In groups (2) and (4), melatonin was freshly diluted with cell medium before application (4 h prior to radiofrequency exposure, at a concentration of 200 nM). Groups (2) and (5) were put into the incubator for sham exposure.
Modulation type: pulsed
ばく露時間: 5 min on - 10 min off - for 24 hr
Exposure to radiofrequency irradiation for a period of 24 h significantly increased the production of reactive oxygen species compared with sham exposure group. Thus, radiofrequency exposure induced oxidative stress in the neurons, and this effect could be reversed by melatonin pretreatment.
At 24 h after exposure, radiofrequency exposure induced a significant increase in the levels of 8-hydroxy-2-deoxyguanosine in the mitochondria of neurons. Concomitant with this finding, the copy number of mitochondrial DNA and the levels of mitochondrial RNA transcripts showed an obvious reduction after radiofrequency exposure. These findings further proved that radiofrequency exposure damaged mitochondrial DNA in neurons. Each of these mitochondrial DNA disturbances could be reversed by pretreatment with the antioxidant melatonin.
The authors conclude that these results suggested that 1800 MHz radiofrequency exposure could cause oxidative damage to mitochondrial DNA in primary cultured neurons.