研究のタイプ: 医学/生物学の研究 (experimental study)

[神経変性疾患のin vitroモデルに対する無線周波数電磁界ばく露の影響] med./bio.

Effect of radiofrequency electromagnetic field exposure on in vitro models of neurodegenerative disease

掲載誌: Bioelectromagnetics 2009; 30 (7): 564-572

この論文は、TEMで発生させた900MHzのGSM信号(SARは1 W/kg)に最大144時間の連続ばく露させた神経細胞のバイアビリティ、増殖、脆弱性を調べた。実験に用いた細胞は、SN56コリン作動性細胞株ラット由来の初代培養皮質ニューロンである。その結果、神経毒性物質との複合ばく露なと特定の条件下においてのみ、GSM変調900MHzへのばく露神経細胞酸化損傷の共ストレッサとして働くことが示唆されたと結論している。

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研究目的(著者による)

To study whether prolonged exposure to 900 MHz GSM modulated electromagnetic fields affects viability and vulnerability of two neural cell cultures: primary cortical neurons (primary culture) and SN56 cell line, co-exposed to 25-35AA beta-amyloid (as in vitro model for Alzheimer disease), to glutamate (as model for excitotoxicity) and to H2O2 (as model for oxidative stress).

詳細情報

The two cell cultures were exposed/co-exposed at different time points (after seeding) and for different durations.

影響評価項目

ばく露

ばく露 パラメータ
ばく露1: 900 MHz
Modulation type: pulsed
ばく露時間: up to 144 h

ばく露1

主たる特性
周波数 900 MHz
タイプ
  • electromagnetic field
ばく露時間 up to 144 h
Modulation
Modulation type pulsed
Repetition frequency 217 Hz
ばく露装置
ばく露の発生源/構造
ばく露装置の詳細 thin inner conductor in the TEM cell provided two symmetrical large regions with field homogeneity; TEM cell placed inside an incubator
Sham exposure A sham exposure was conducted.
パラメータ
測定量 種別 Method Mass 備考
SAR 1 W/kg - - - -

Reference articles

ばく露を受けた生物:

方法 影響評価項目/測定パラメータ/方法

研究対象とした生物試料:
調査の時期:
  • ばく露後

研究の主なアウトカム(著者による)

The data showed that radiofrequency exposure did not change cell viability and proliferation rate of the SN56 cholinergic cells or viability of cortical neurons. Co-exposure to radiofrequency exacerbated neurotoxic effect of hydrogen peroxide in SN56 cells, but not in primary cortical neurons, whereas no cooperative effects of radiofrequency exposure with glutamate and 25-35AA beta amyloid were found.
These findings suggest that only under particular circumstances exposure to GSM modulated, 900 MHz signal act as a co-stressor for oxidative damage of neural cells.

研究の種別:

研究助成

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