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Electromagnetic fields act via activation of voltage-gated calcium channels to produce beneficial or adverse effects

机译:电磁场通过激活电压门控钙通道起作用产生有利或不利影响

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摘要

The direct targets of extremely low and microwave frequency range electromagnetic fields (EMFs) in producing non-thermal effects have not been clearly established. However, studies in the literature, reviewed here, provide substantial support for such direct targets. Twenty-three studies have shown that voltage-gated calcium channels (VGCCs) produce these and other EMF effects, such that the L-type or other VGCC blockers block or greatly lower diverse EMF effects. Furthermore, the voltage-gated properties of these channels may provide biophysically plausible mechanisms for EMF biological effects. Downstream responses of such EMF exposures may be mediated through Ca2+/calmodulin stimulation of nitric oxide synthesis. Potentially, physiological/therapeutic responses may be largely as a result of nitric oxide-cGMP-protein kinase G pathway stimulation. A well-studied example of such an apparent therapeutic response, EMF stimulation of bone growth, appears to work along this pathway. However, pathophysiological responses to EMFs may be as a result of nitric oxide-peroxynitrite-oxidative stress pathway of action. A single such well-documented example, EMF induction of DNA single-strand breaks in cells, as measured by alkaline comet assays, is reviewed here. Such single-strand breaks are known to be produced through the action of this pathway. Data on the mechanism of EMF induction of such breaks are limited; what data are available support this proposed mechanism. Other Ca2+-mediated regulatory changes, independent of nitric oxide, may also have roles. This article reviews, then, a substantially supported set of targets, VGCCs, whose stimulation produces non-thermal EMF responses by humans/higher animals with downstream effects involving Ca2+/calmodulin-dependent nitric oxide increases, which may explain therapeutic and pathophysiological effects.
机译:在产生非热效应方面,极低和微波频率范围电磁场(EMF)的直接目标尚未明确建立。但是,这里回顾的文献研究为此类直接目标提供了实质性支持。二十三项研究表明,电压门控钙离子通道(VGCC)会产生这些和其他EMF效应,因此L型或其他VGCC阻滞剂会阻止或大大降低各种EMF效应。此外,这些通道的电压门控特性可以为EMF生物学效应提供生物物理上合理的机制。此类EMF暴露的下游响应可能是通过Ca 2 + /钙调蛋白刺激一氧化氮合成而介导的。潜在地,生理/治疗反应可能主要是一氧化氮-cGMP-蛋白激酶G途径刺激的结果。研究人员充分研究了这种明显的治疗反应,即EMF刺激骨生长,似乎沿该途径起作用。然而,对EMF的病理生理反应可能是一氧化氮-过氧亚硝酸盐-氧化应激作用途径的结果。本文回顾了一个如此有据可查的例子,即通过碱性彗星试验测定的EMF诱导细胞中DNA单链断裂的方法。已知这种单链断裂是通过该途径的作用产生的。关于EMF诱导此类断裂的机理的数据有限;有哪些可用数据支持此提议的机制。 Ca 2 + 介导的其他调节变化,独立于一氧化氮,也可能起作用。然后,本文回顾了一组基本受支持的靶标VGCC,其刺激会引起人/高等动物的非热EMF反应,并产生涉及Ca 2 + /钙调蛋白依赖性一氧化氮的下游效应,这可以解释治疗和病理生理作用。

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