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

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

Lawrence A. Plumlee-2
Review Article J. Cell. Mol. Med. Vol XX, No X, 2013 pp. 1-9
                                      Guest Editor:
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

Complete Article Free at
<http://onlinelibrary.wiley.com/doi/10.1111/jcmm.12088/pdf>http://onlinelibrary.wiley.com/doi/10.1111/jcmm.12088/pdf

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 channels low frequency electromagnetic
field exposure nitric oxide oxidative stress calcium channel blockers

Continued at
<http://onlinelibrary.wiley.com/doi/10.1111/jcmm.12088/pdf>http://onlinelibrary.wiley.com/doi/10.1111/jcmm.12088/<http://onlinelibrary.wiley.com/doi/10.1111/jcmm.12088/pdf>pdf



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Re: Taurine is a good Calcium Channel Blocker

Hud J O Ramelan
As far as I recall, taurine is an L-type calcium channel blocker.  Magnesium and manganese are also CCBs--probably not L-type CCBs but I'm not sure.

 

  ~=~
  Hud
_________________________________________________________
nam tua res agitur, paries cum proximus ardet
You too are in danger when your neighbor's house is on fire (Horace)




>________________________________
> From: Lawrence A. Plumlee <[hidden email]>
>To: [hidden email]
>Sent: Thursday, July 18, 2013 9:59:12 PM
>Subject: [eSens] AAEM News: TEP: Electromagnetic fields act via activation of  voltage-gated calcium channels to produce beneficial or adverse effects
>
>
>Review Article J. Cell. Mol. Med. Vol XX, No X, 2013 pp. 1-9
>                                      Guest Editor:
>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
>
>,omplete Article Free at
><http://onlinelibrary.wiley.com/doi/10.1111/jcmm.12088/pdf>http://onlinelibrary.wiley.com/doi/10.1111/jcmm.12088/pdf
>
>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 channels low frequency electromagnetic
>field exposure nitric oxide oxidative stress calcium channel blockers
>
>Continued at
><http://onlinelibrary.wiley.com/doi/10.1111/jcmm.12088/pdf>http://onlinelibrary.wiley.com/doi/10.1111/jcmm.12088/<http://onlinelibrary.wiley.com/doi/10.1111/jcmm.12088/pdf>pdf
>
>
>
>[Non-text portions of this message have been removed]
>
>
>
>------------------------------------
>
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[Non-text portions of this message have been removed]