この研究は、培養内皮細胞に電磁界(EMF)のばく露を与え、それによって強力な血管収縮剤であるエンドセリン-1(ET-1)の産生が変化するか否かを調べた。実験にはいくつかの種類の培養内皮細胞を用いた。結果として、ヒトの臍静脈および微小血管の内皮細胞においては、EMFばく露によりET-1の基礎レベルが低下した;一方、ウシおよびヒトの大動脈の内皮細胞においては、ET-1の基礎レベルはEMFばく露によって変化しなかった;4種類すべての内皮細胞のトロンビン刺激性ET-1産生は、EMFばく露量に依存して有意に抑制された;また、4種類すべての内皮細胞において、トロンビン誘発エンドセリン1 mRNA発現がEMFばく露により有意に抑制された;ET-1生産に対するEMFばく露による抑制効果は、一酸化窒素合成酵素阻害剤NG-モノメチル-L-アルギニン(10(-3)mol / 1)により消失した、と報告している。
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To study the effect of radiofrequency electromagnetic field on basal and thrombin-stimulated endothelin-1 (a potent vasoconstrictor) expression and production in cultured cells from a variety of sources (bovine aortic endothelial cells, human umbilical vascular endothelial cells, human aortic endothelial cells, and human microvascular endothelial cells).
Electromagnetic field exposure has been found to induce arteriolar dilatation, but the mechanism of action remains largely unknown.
To study whether nitric oxide may participate in the mediation of endothelin-1 production by electromagnetic field, a competitive inhibitor of nitric oxide synthase (NG-monomethyl-L-arginine) was used to block the synthesis of nitric oxide in the cell cultures.
周波数 | 10 MHz |
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ばく露時間 | continuous for 8 h or 24 h |
Modulation type | pulsed |
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Duty cycle | 50 % |
Repetition frequency | 10,000 Hz |
ばく露の発生源/構造 |
|
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ばく露装置の詳細 | 96 well culture plates containing endothelial cells were placed on a coil plate. Cells were sham exposed for the same duration under the same set-up conditions. |
Additional information | The distance between the generator coil and the cells was 2.0 mm. |
周波数 | 10 MHz |
---|---|
ばく露時間 | continuous for 8 h or 24 h |
Modulation type | pulsed |
---|---|
Duty cycle | 50 % |
Repetition frequency | 10,000 Hz |
ばく露の発生源/構造 |
|
---|---|
ばく露装置の詳細 | 100 mm culture dish containing endothelial cells was placed on a coil plate. Cells were sham exposed for the same duration under the same set-up conditions. |
Additional information | The distance between the generator coil and the cells was 2.3 mm. |
Electromagnetic field exposure reduced endothelin-1 basal levels in human umbilical vein and microvascular endothelial cells, but failed to reduce endothelin-1 basal levels in bovine and human aortic endothelial cells.
Electromagnetic field exposure significantly inhibited thrombin-stimulated (thrombin up-regulates the endothelin-1 production) endothelin-1 production in all four endothelial cell types in a dose-dependent manner.
Electromagnetic field irradiation significantly inhibited thrombin-induced endothelin-1 mRNA expression in all four cell types.
The inhibitory effect on endothelin-1 production was abolished by the nitric oxide synthase inhibitor.
These findings demonstrate that electromagnetic field exposure modulates endothelin-1 production in cultured vascular endothelial cells and the inhibitory effect is, at least partly, mediated through a nitric oxide-related pathway.
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