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Pall: EMV effecten via activering van 'voltage-gated' Ca kanalen    
Ga naar overzicht berichten in: Onderzoeken

Pall: EMV effecten via activering van 'voltage-gated' Ca kanalen
zaterdag, 31 augustus 2013 - Dossier: Algemeen


Bron:
www.ncbi.nlm.nih.gov/pmc/articles/PMC3780531/ .
aug 2013


Review Article
J Cell Mol Med. Aug 2013; 17(8): 958–965.
Published online Jun 26, 2013. doi: 10.1111/jcmm.12088

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


Martin L. Pall *
Professor Emeritus of Biochemistry and Basic Medical Sciences, Washington State University, Portland, OR, USA
Received: January 8, 2013; Accepted: May 20, 2013

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 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.

Keywords: intracellular Ca2+ voltage-gated calcium channelslow frequency electromagnetic field exposurenitric
oxideoxidative stresscalcium channel blockers

Voor het volledige artikel zie bovenstaande pdf link en een nadere uitleg van Prof. Olle Johansson hieronder.

From: Olle Johansson

Date: Fri, Jul 19, 2013 at 4:58 PM

Subject: A new paper by professor Martin Pall, a must read!
''Electromagnetic fields act via activation of voltage-gated calcium
channels to produce beneficial or adverse effects''

One of the great puzzles about the action of electromagnetic fields is how can they influence the biology of our bodies? The reason that this is such a great puzzle is that these fields are comprised of low energy photons, with energies too low to influence the chemistry of our bodies. So how can they possibly influence our biology? Many have argued that the only thing that they can possibly do is to heat things, and yet it is very clear that levels of exposure that produce only the slightest heating have been repeatedly shown to produce substantial biological effects. Now this puzzle has been solved in a paper with the title of this email, published on line in the Journal of Cellular and Molecular Medicine, freely available on the publisher's web site:

That paper reviews 24 different studies in which EMF exposures produce biological effects that can be blocked by using calcium channel blockers, drugs that block the action of voltage-gated calcium channels (VGCCs). Most of these drug studies implicated L-type VGGCs, showing blockage by channel blockers specific for these L-type VGCCs; however three other classes of the voltage gated calcium channels were also implicated in some of these studies. What these and other studies show, is that EMF exposures act by partially depolarizing the electrical charge across the plasma membrane of cells, activating the VGCCs and it is the increased intracellular calcium levels that are responsible for the reaction to EMF exposure. These 24 studies implicate the VGCCs in responses to a variety of EMFs, including extremely low frequency EMFs such as 50 and 60 cycle fields produced by our alternating currents in our wiring, various microwave/radiofrequency EMFs and nanosecond electrical pulses. Static electrical fields also act via VGCCs, not surprisingly because they also influence the electrical charge across plasma membranes.
Perhaps more surprisingly, static magnetic fields also act via VGCCs. This is a bit surprising because static magnetic fields do not produce electrical changes in static objects. However as pointed out in the paper, living cells in the body are rarely static, often moving rapidly in such phenomena as cellular ruffling.

Having resolved this long-standing puzzle, the paper goes on to consider how VGCC activation can produce two well-documented responses to EMF exposure: stimulating of bone growth and the production of single stranded DNA breaks in EMF-exposed cells. EMF exposures have repeatedly been shown to produce increases in nitric oxide levels, in some cases almost instantaneously. These nitric oxide increases are produced through calcium stimulation of the action of the two nitric oxide synthases in the cell, iNOS and eNOS, which are both calcium dependent enzymes. Nitric oxide in the cell, acts to produce most physiological effects, by stimulating the production of cycle GMP which stimulates, in turn the G-kinase (this is known as the NO/sGC/cGMP/G kinase pathway). Most pathophysiological responses to nitric oxide to through another pathway, where nitric oxide acts as a precursor of peroxynitrite, a potent oxidant and reactive free radical precursor. The paper suggests that the EMF stimulation of bone growth, a very promising therapeutic response, goes through the first pathway. It also suggests that induction of single strand breaks in cellular DNA goes through the second pathway. It is possible that possible beneficial effects of EMFs go through the first pathway and adverse, pathophysiological effects go through the second pathway.
Clearly we will need a lot of study to test mechanisms of EMF action.

This paper may be viewed in a practical setting as being very important in two ways:

1. There have been many claims that biological effects of EMF exposures cannot possibly exist because no plausible mechanism of action of such exposures could produce such effects. Clearly these claims are now defunct.

2. In studies aimed at understanding the mechanisms of action of EMF exposures we now know where to look. Such studies need to look at roles of VGCCs, intracellular calcium, nitric oxide and possibly cycle GMP or peroxynitrite. It can be argued, therefore, that this paper is very much a game changer, changing a situation where there has been substantial confusion, into one where, specific, targeted questions can be asked and answered experimentally.

Finally, this paper says nothing at all about EMF hypersensitivity (often abbreviated EHS), a condition where previous EMF exposure appears to induce high level sensitivity to some types of EMFs. EHS is similar to multiple chemical sensitivity (MCS), where previous chemical exposures produce high level chemical sensitivity. Chemicals act in MCS by indirectly activating the NMDA receptors and NMDA receptors have many similarities in their properties to those of the L-type VGCCs. You should expect, therefore, a future paper on a detailed proposed mechanism for EHS, with both many similarities and some apparent mechanism of MCS as well as some differences.


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