Autoimmune processes after long-term low-level exposure to electromagnetic fields part 4. Oxidative intracellular stress response to the long-term rat exposure to nonthermal RF EMF

Михайлов, В. Ф.; Ivanov, А.А.; Mal'tsev, V N; Ulanova, A.M.; Ставракова, Н. М.; Николаева, И. А.; Grigoriev, O. A.

doi:10.1134/s0006350910060308

Cited by 2 publications

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“…Peroxynitrite elevation is usually measured through a marker of peroxynitrite-mediated protein nitration, 3-nitrotyrosine (3-NT). There are four studies where 3-NT levels were measured before and after EMF exposure [66,[68][69][70]. Each of these studies provides some evidence supporting the view that EMF exposure increases levels of peroxynitrite and therefore 3-NT levels [66,[68][69][70].…”

Section: Possible Modes Of Action Following Vgcc Stimulationmentioning

confidence: 88%

“…There are four studies where 3-NT levels were measured before and after EMF exposure [66,[68][69][70]. Each of these studies provides some evidence supporting the view that EMF exposure increases levels of peroxynitrite and therefore 3-NT levels [66,[68][69][70]. Although these cannot be taken as definitive, when considered along with the evidence on oxidative stress and elevated nitric oxide production in response to EMF exposure, they strongly suggest a peroxynitritemediated mechanism of oxidative stress in response to EMFs.…”

Section: Possible Modes Of Action Following Vgcc Stimulationmentioning

confidence: 96%

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

Pall

2013

J Cellular Molecular Medi

354

234

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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.

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