目的と方法:ショウジョウバエをモデル動物とした実験系で、携帯電話の835MHz電磁界による生物学的影響を調べること。結果:米国規格協会(ANSI)のばく露制限値である比吸収率(SAR)値1.6 W/kgにショウジョウバエをばく露させた場合、30時間ばく露の後であっても、その90%が生存していた。しかし、SAR値4.0 W/kgの場合、12時間ばく露から生存率は低下し始めた。電磁界ばく露はストレス反応の引き金となり、活性酸素種の生成を増加させた。また、電磁界ばく露は細胞外信号制御キナーゼ(ERK)とc - Jun N末端キナーゼ(JNK)を活性化させたが、p38キナーゼのシグナリングは活性化されなかった。具体的には、SAR値1.6 W/kgの時には、主にERKシグナリングと抗アポトーシス遺伝子発現が活性化されたが、SAR値4.0W/kgの時には、JNKシグナリングとアポトーシス遺伝子発現が強く活性化された。加えて、SAR値4.0W/kgにおいては、ハエの脳でアポトーシス細胞数が増えた。結論:ショウジョウバエにおいて、ANAIが提唱する電磁界放射のばく露制限値は、ERKの生存シグナリングを引き起こしたが、それより強い電磁界放射はJNKの細胞死シグナリングを活性化した。
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This study was performed to understand the molecular nature of the biological effects of mobile phone electromagnetic field at the organism level of the fruit fly.
A total of 690 adult female flies, wild type or mutants, were exposed at two different specific absorption rates: at 1.6 W/kg representing the exposure limit proposed by the American National Standards Institute (ANSI) and at 4 W/kg. At least three independent experiments were performed in each electromagnetic field exposure condition. To prove whether decreased viability after exposure is related to changed anti-oxidant status two transgenic mutant flies exhibiting defective superoxide dismutase were crossed (Actin5C-Gal4 and UAS-SOD1IR or UAS-SOD2IR).
周波数 | 835 MHz |
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タイプ |
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特性 |
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ばく露時間 | continuous for 6, 12, 18, 24, 30, and 36 h |
ばく露の発生源/構造 |
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チャンバの詳細 | The exposure device was placed in a chamber maintained at 25 ± 0.1 °C to avoid thermal effects. |
ばく露装置の詳細 | Flies were exposed in the device in a 100-mm Petri dish with a wet filter paper to maintain humidity. |
Additional information | At least three independent experiments were performed in each exposure condition. |
At the specific absorption rate 1.6 W/kg, more than 90% of the flies were viable even after the 30 hours exposure. However, at the specific absorption rate 4 W/kg, viability was decreasing from the 12 hours exposure. Only 10% of the flies survived after the 30 hours exposure.
The exposure significantly increased intercellular ROS levels by time and intensity. Superoxide dismutase defect mutants showed lower viability compared to the wild type.
The electromagnetic field exposures activated ERK and JNK signal transduction pathway, but not p38 kinase signal transduction pathway. Interestingly, the specific absorption rate 1.6 W/kg activated mainly ERK signal transduction pathway and expression of an anti-apoptotic gene, whereas the specific absorption rate 4 W/kg strongly activated JNK signal transduction pathway and expression of apoptotic genes.
In addition, the specific absorption rate 4 W/kg amplified the number of apoptotic cells in the fly brain.
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