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

[人為的な無線周波電磁界は切断モデルに神経因性疼痛を引き起こす] retracted

Anthropogenic Radio-Frequency Electromagnetic Fields Elicit Neuropathic Pain in an Amputation Model (RETRACTED).

掲載誌: PLoS One 2016; 11 (1): e0144268

この研究は、神経障害性痛のTNTモデル(ラット脛骨神経を末梢で切断し、皮下に神経断端を移行させた動物モデル)において、無線周波電磁界RF EMFs)が神経因性疼痛を生じさせるか否かを実験で調べた。その結果、擬似的外科手術群に比べ、TNTモデル群ではRF EMFsに対する有意で持続的な痛み反応が生じることが、行動試験により示唆された;加熱用赤外線ランプに対しても痛み反応が観察されたが、RF EMFsに対する反応の頻度や進行には及ばなかった、と報告している。

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研究目的(著者による)

The effects of exposure of rats to a 915 MHz electromagnetic field (EMF) on neuropathic pain in an amputation model should be investigated, as few studies (Yuh et al. 1992, Formica et al. 2004 and Colip 2013) have suggested an association between EMF and neuropathic pain.

詳細情報

Neuropathic pain is pain caused by damage of the nervous system, e.g. caused by an amputation.
From a total of 20 rats, 16 were randomly selected to receive a surgical treatment to simulate amputation and generate a neuroma (a neural bulb typically occurring after amputations) at the sciatic nerve (TNT group). The remaining animals (n=4) received sham surgeries (TNT sham group). Both groups were exposed to the electromagnetic field afterwards (remark EMF-Portal: there was no control group and no statistical comparisons to a control condition without exposure were made).
After 4 weeks of exposure, animals from the TNT group were randomly divided into two subgroups (n=8 each): 1) TNT neuroma resection and 2) TNT sham resection. Moreover, 8-week-old neuromas of unspecified origin were investigated.
To check whether the pain response was caused by thermal effects, additional tests with an infrared heat source were conducted.
In parallel, in vitro experiments were conducted on dissociated dorsal root ganglion neurons in the presence and absence of TNF-α (to simulate the conditions of inflammatory injury) in order to determine whether exposure to EMF was sufficient to directly depolarize sensory neurons.

影響評価項目

ばく露

ばく露 パラメータ
ばく露1: 915 MHz
ばく露時間: continuous for 10 minutes once peer week for 8 weeks in a row and once in week 28
in vivo experiments
  • 電力密度: 756 mW/m² average over time (maximum value, ± 8.5 mW/m2)
  • SAR: 0.36 W/kg (at the skin surface)
  • 電界強度: 21.5 V/m (± 0.1 V/m)
ばく露2: 915 MHz
ばく露時間: continuous for 10 minutes
in vitro experiments
  • 電力密度: 756 mW/m² average over time (maximum value, ± 8.5 mW/m2)

ばく露1

主たる特性
周波数 915 MHz
偏波
  • circular
ばく露時間 continuous for 10 minutes once peer week for 8 weeks in a row and once in week 28
Additional information in vivo experiments
ばく露装置
ばく露の発生源/構造
Distance between exposed object and exposure source 25.4 cm
チャンバの詳細 clear acrylic box with ample clearance for air exchange
ばく露装置の詳細 no further specifications
Sham exposure A sham exposure was conducted.
パラメータ
測定量 種別 Method Mass 備考
電力密度 756 mW/m² average over time 測定値 - maximum value, ± 8.5 mW/m2
SAR 0.36 W/kg - - - at the skin surface
電界強度 21.5 V/m - 測定値 - ± 0.1 V/m

ばく露2

主たる特性
周波数 915 MHz
偏波
  • circular
ばく露時間 continuous for 10 minutes
Additional information in vitro experiments
ばく露装置
ばく露の発生源/構造
  • RF antenna
チャンバの詳細 glass-bottomed 35 mm culture dishes in incubator with 37°C and 5% CO2
ばく露装置の詳細 antenna was fixed approximately 6 inches above the incubator
Sham exposure A sham exposure was conducted.
パラメータ
測定量 種別 Method Mass 備考
電力密度 756 mW/m² average over time 測定値 - maximum value, ± 8.5 mW/m2

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:
研究対象とした臓器系:
  • peripheral nervous system
調査の時期:
  • ばく露前
  • ばく露中
  • ばく露後

研究の主なアウトカム(著者による)

During exposure to the electromagnetic field, a significant higher pain response was observed in the TNT group compared to the TNT sham group from week 3, what could not be prevented by resection of neuroma bulbs. An injection of lidocaine prevented pain, which indicated a nerve-mediated pain reaction. During exposure in the pretest, the skin temperature increased by 2.1 ± 0.7°C (remark EMF-Portal: the comparability to mobile radio exposure is questionable).
Exposure to the thermal stimulus increased the skin temperature by 4.8 ± 0.4°C and induced a significantly higher pain response in the TNT group compared to the TNT sham group as well. However, this response was lower compared to EMF exposure, indicating a thermal component in EMF-induced pain but also additional mechanisms.
In neuroma bulbs, a significantly increased protein expression of TRPV4 ion channels compared to the contralateral healthy nerve was found. This indicated that EMF-induced postamputation pain may be mediated by activation of TRPV4 ion channels.
In the in vitro experiments, EMF-exposed cells showed significantly higher rates of intracellular calcium peaks compared to the control group, which was interpreted as indicative of an effect on depolarization and activation of the neurons. Administration of TNF-α resulted in a significantly higher percentage of activated neurons during EMF exposure, suggesting an increased sensitivity of sensory neurons through EMF exposure in combination with inflammatory processes.
The authors conclude that exposure of rats to a 915 MHz electromagnetic field might contribute to neuropathic pain in an amputation model.

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