Electromagnetic fields act via activation of voltage-gated calcium channels to produce beneficial or adverse effects.
Pall ML.
J Cell Mol Med. 2013 ;17(8):958-65.
Professor Emeritus of Biochemistry and Basic Medical Sciences, Washington State University, Portland, OR, USA. martin_pall@wsu.edu
Abstract
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 Ca(2+) /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 Ca(2+) -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 Ca(2+) /calmodulin-dependent nitric oxide increases, which may explain therapeutic and pathophysiological effects.
© 2013 The Author. Journal of Cellular and Molecular Medicine Published by Foundation for Cellular and Molecular Medicine/Blackwell Publishing Ltd
Additional Information
This paper showed that three widely reported effects of microwave EMF exposure can be produced by known mechanisms as downstream effects of EMF-produced VGCC activation, notably therapeutic effects, single stranded breaks in DNA and oxidative stress. I recently submitted a paper showing that other repeatedly reported effects of low level microwave EMF exposures can also be produced via known mechanisms from downstream effects of VGCC activation. These include: Double strand breaks in DNA, as measured by micronucleus formation; cancer via the same mechanism that causes inflammatory carcinogenesis; male and female infertility; breakdown of the blood-brain barrier; greatly lowered melatonin levels leading to sleep dysfunction. Other less frequently reported responses including multiple types of brain dysfunction and aberrant electrical control of the heart, including tachycardia, arrhythmia and sudden cardiac death can also be produced by downstream effects of VGCC activation. It appears, therefore, that EMF action via VGCC activation is likely to be a very important integrative concept in EMF-induced pathophysiology.
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