EMF EXPERTS DISCUSS EMFS AND VGCCS
From: Joel MOSKOWITZ
On 2015-03-18 à 05:48, Pall, Martin L wrote:
On 2015-03-18 at 19:19, Martin Blank wrote:
On 2015-03-20 à 08:13, Dariusz Leszczynski wrote :
"Pall, Martin L"
On 2015-03-21 à 09:08, D L Henshaw a écrit :
Le 2015-03-21 à 23:43, Henry Lai a écrit :
From: "Dariusz Leszczynski"
From: "Dimitris Panagopoulos"
From: Martin Blank
Object: Rép : California knew smart meters were dangerous (url of my English summary)
Date: Aprl 1 2015 01:09:20 UTC−4
Response to Martin Pall’s March 26 email
Martin Pall’s March 26 email provided many examples of the effect of EMF on Ca-transporting systems. However, the question is whether one can designate this as the initial interaction of EMF with cells that initiates a chain of reactions. After all, EMF interacts with many cellular systems, and judging from the earlier studies of Lai and Singh (Int. J. Radiat. Biol. 69:513–521, 1996), one would certainly expect interactions with the DNA in cells.Goodman and Blank (Adv in Chemistry 250:423-436, 1995; Cell Stress & Chaperones 3:79-88, 1998) showed EMF interaction with DNA to initiate the cellular stress response and synthesis of stress protein hsp70. They also identified a combination of DNA bases that EMF interacts with, suggesting that there are bound to be many places on the two meter long molecule that have this combination and can interact (Lin, Blank, Rossol-Haseroth and Goodman, J Cell Biochem 81:143-148, 2001). Because of the extensive coiling of DNA needed to enable the molecule to fit into the nucleus, there are coils of many sizes. The coiling of DNA provides a structural basis for why DNA acts as a fractal antenna (Blank and Goodman, Internat. J. Radiation Biol 87: 409-15, 2011). The different size coils in the DNA interact with different EMF wave lengths.The DNA research has important practical implications:· * The cellular stress response is the cell’s reaction to a variety of potentially harmful stimuli (e.g., changes in temperature, pH, etc.), and indicates that EMF is a potentially harmful stimulus according to the biological criterion.· * The threshold for response to EMF is lower than for changes in temperature, i.e., ‘heat shock’. This shows that the ‘thermal criterion’ for judging EMF safety for cells is incorrect according to the ‘biological criterion’.· * This also shows that despite the claims of regulatory agencies, there is a recognized cell-EMF interaction mechanism.· * It is important for regulatory agencies considering EMF safety issues to include biologists who are familiar with relevant cell biology research.
De: "Pall, Martin L"Objet: RE: Response to Martin Blank’s April 1 emailDate: 4 avril 2015 21:07:33 UTC−4À: André FauteuxDear Martin Blank:Thank you for your thoughtful and substantive response to my earlier message - it is much appreciated and I have spent considerable time going over the relevant papers. Let me reiterate that the question I am raising is whether VGCC activation and downstream effects produced by such activation can explain the important experimental results that you have obtained - or not. I have posted that the activation of the heat shock transcription factor can be produced by excessive intracellular calcium levels and that this response to [Ca2+]i has been found in diverse eukaryotic organisms including diverse animals (including Drosophila and Ceanorhabditis and both vertebrates and other invertebrates) , higher plants and in yeast. What you show is that the stress response you have been studying is produced in part via heat shock transcription factor activation and in part via other mechanisms. What you also show is that you have a plausible mechanism based on the direct interaction of EMFs with DNA which may explain, at least in part, your studies. The question is whether this plausible mechanism is fundamentally correct.You have evidence that several other transcription factors are activated EMF exposures, notably Ap-1, Ap-2, and Sp-1. Ap-1 is, of course, well known to be activated by oxidants and therefore, may be expected to be activated by the peroxynitrite/free radical/oxidative stress pathway that is an important downstream pathway of VGCC activation and consequent elevation of [Ca2+]i. I don't know enough about Ap-2 and Sp-1 to comment on them. Calcium, of course has important roles in transcriptional regulation and activation of the L-type VGCCs was shown to have a direct important role in transcriptional regulation as well, a role in addition to its role in increasing [Ca2+]i (see Dolmetsch et al, Science 2001;294(5541):333-339). Other possible effects that are downstream of VGCC activation involves the known role of elevated peroxynitrite, acting through its free radical breakdown products, in producing both single strand and double strand breaks in DNA, a mechanism discussed in my 2013 EMF paper. That paper also discusses an important flaw in the Friedman paper which concluded that NADH oxidase was the source of oxidants following EMF exposure - the "specific" NADH oxidase inhibitor is, in fact not specific, but rather is also an ion channel blocker, raising the question of whether peroxynitrite is the main source of oxidants following exposures, rather than NADH oxidase. One of the consequences of DNA strand breaks is that they produce a major activation of poly-ADP-ribosylation of chromosomal proteins which can both have major effects on chromosome and therefore DNA structure and can also lead to a depletion of NAD/NADH pools, with the NADH effect, leading to greatly lowered energy metabolism. All of these things can produce major stresses on the cell, and therefore in principle, each could have a role in the stress response that you have been studying.The 5 calcium channel blockers that have been used in the VGCC studies each act on different sites and are each thought to be highly specific of VGCC blockage, although they are each specific for one of 4 different families of VGCCs. So we have strong evidence for a causal role of the VGCCs in responding to the fields. We also have the Pilla 2012 study which showed that the VGCCs are activated almost instantaneously by the EMFs, producing an almost instantaneous increase in calcium/calmodulin-dependent NO synthesis. And we know that the VGCCs and the other voltage-gated ion channels each have a voltage sensor which I have argued is exquisitely sensitive to EMFs - and the voltage sensor of the VGCCs has a universal or near universal role in converting electrical effects into chemical changes in the cell. I am going to email you directly a paper that considers many of these issues including the voltage sensor properties.It seems to me that we each have a plausible set of mechanisms leading to the stress response you are studying - so my question for you is whether you see any definitive evidence that DNA is the EMF target leading to those stress responses?One other thing, I think that your last section in the DNA fractals paper, on implications for safety standards, is absolutely bang on. The safety standards are off by orders of magnitude from where they need to be. Whatever differences we may have on the issue of mechanism should not detract from our fundamental agreement that the ICNIRP and other safety standards are without scientific merit.Martin Pall