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      Searching for the Perfect Wave: The Effect of Radiofrequency Electromagnetic Fields on Cells

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          Abstract

          There is a growing concern in the population about the effects that environmental exposure to any source of “uncontrolled” radiation may have on public health. Anxiety arises from the controversial knowledge about the effect of electromagnetic field (EMF) exposure to cells and organisms but most of all concerning the possible causal relation to human diseases. Here we reviewed those in vitro and in vivo and epidemiological works that gave a new insight about the effect of radio frequency (RF) exposure, relating to intracellular molecular pathways that lead to biological and functional outcomes. It appears that a thorough application of standardized protocols is the key to reliable data acquisition and interpretation that could contribute a clearer picture for scientists and lay public. Moreover, specific tuning of experimental and clinical RF exposure might lead to beneficial health effects.

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

          Martin L Pall (2013)
          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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            Epidemiology and etiology of Alzheimer's disease: from genetic to non-genetic factors.

            Teng Jiang, Jin-Tai Yu, Yan Tian … (2013)
            At present, the etiology of Alzheimer's disease (AD) is still unclear, but both genetic and non-genetic factors are thought to take part in the etiopathogenesis of AD. Epidemiologic researches revealed that genetic factors played a decisive role in the development of both early-onset AD (EOAD) and late-onset AD (LOAD). The mutations in APP, PSEN1 and PSEN2 are inherited in a Mendelian fashion and directly lead to the EOAD, while recent genome-wide association studies have identified numbers of risky genes, which influences the susceptibility to LOAD. Although genetic factors are inherited and fixed, non-genetic factors, such as occupational exposures (exposure to pesticides, electromagnetic fields, organic solvents and volatile anesthetics), pre-existing medical conditions (cerebrovascular disease, hypertension, diabetes, dyslipidemia, traumatic brain injury, depression and cancer) and lifestyle factors (smoking, consumptions of alcohol and coffee, body mass index, physical activity and cognitive activity), are partly environmentally-determined. Timely interventions targeted at these non-genetic risk factors may offer opportunities for prevention and treatment of AD. In the future, more high-quality and large-sample epidemiologic studies are needed to identify risk factors for AD, and the interaction models between genetic and non-genetic risk factors required further investigation. In addition, public health campaigns targeted at modification of non-genetic risk factors should be developed among population at high risk of AD.
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              A Comparative Analysis of the In Vitro Effects of Pulsed Electromagnetic Field Treatment on Osteogenic Differentiation of Two Different Mesenchymal Cell Lineages

              Gabriele Ceccarelli, Nora Bloise, Melissa Mantelli … (2013)
              Abstract Human mesenchymal stem cells (MSCs) are a promising candidate cell type for regenerative medicine and tissue engineering applications. Exposure of MSCs to physical stimuli favors early and rapid activation of the tissue repair process. In this study we investigated the in vitro effects of pulsed electromagnetic field (PEMF) treatment on the proliferation and osteogenic differentiation of bone marrow MSCs (BM-MSCs) and adipose-tissue MSCs (ASCs), to assess if both types of MSCs could be indifferently used in combination with PEMF exposure for bone tissue healing. We compared the cell viability, cell matrix distribution, and calcified matrix production in unstimulated and PEMF-stimulated (magnetic field: 2 mT, amplitude: 5 mV) mesenchymal cell lineages. After PEMF exposure, in comparison with ASCs, BM-MSCs showed an increase in cell proliferation (p<0.05) and an enhanced deposition of extracellular matrix components such as decorin, fibronectin, osteocalcin, osteonectin, osteopontin, and type-I and -III collagens (p<0.05). Calcium deposition was 1.5-fold greater in BM-MSC–derived osteoblasts (p<0.05). The immunofluorescence related to the deposition of bone matrix proteins and calcium showed their colocalization to the cell-rich areas for both types of MSC-derived osteoblast. Alkaline phosphatase activity increased nearly 2-fold (p<0.001) and its protein content was 1.2-fold higher in osteoblasts derived from BM-MSCs. The quantitative reverse-transcription polymerase chain reaction (qRT-PCR) analysis revealed up-regulated transcription specific for bone sialoprotein, osteopontin, osteonectin, and Runx2, but at a higher level for cells differentiated from BM-MSCs. All together these results suggest that PEMF promotion of bone extracellular matrix deposition is more efficient in osteoblasts differentiated from BM-MSCs.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Int J Mol Sci
                Journal ID (iso-abbrev): Int J Mol Sci
                Journal ID (publisher-id): ijms
                Title: International Journal of Molecular Sciences
                Publisher: Molecular Diversity Preservation International (MDPI)
                ISSN (Electronic): 1422-0067
                Publication date Collection: April 2014
                Publication date (Electronic): 27 March 2014
                Volume: 15
                Issue: 4
                Pages: 5366-5387
                Affiliations
                [1 ]Institute of Clinical Physiology, Consiglio Nazionale delle Ricerche Siena, Strada Petriccio e Belriguardo, Siena 53100, Italy; E-Mail: lghera@ 123456gmail.com
                [2 ]The BioRobotics Institute, Scuola Superiore Sant’Anna, Viale Rinaldo Piaggio 34, Pisa 56025, Italy; E-Mails: g.ciuti@ 123456sssup.it (G.C.); s.tognarelli@ 123456sssup.it (S.T.)
                Author notes
                [* ]Author to whom correspondence should be addressed; E-Mail: ccinti@ 123456ifc.cnr.it ; Tel.: +39-0577-381295; Fax: +39-0577-381298.
                Article
                Publisher ID: ijms-15-05366
                DOI: 10.3390/ijms15045366
                PMC ID: 4013569
                PubMed ID: 24681584
                SO-VID: cf62c3b1-0d4b-4eca-8c05-b9953be8e87b
                Copyright © © 2014 by the authors; licensee MDPI, Basel, Switzerland
                License:

                This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution license ( http://creativecommons.org/licenses/by/3.0/).

                History
                Date received : 03 December 2013
                Date revision received : 17 January 2014
                Date accepted : 20 March 2014
                Categories
                Subject: Review

                ScienceOpen disciplines: Molecular biology
                Keywords: radio frequencies,neurodegeneration,radiotoxicity,cancer
                Data availability:
                ScienceOpen disciplines: Molecular biology
                Keywords: radio frequencies, neurodegeneration, radiotoxicity, cancer

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