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(Database last updated on Mar 27, 2024)
| ID Number | 1161 | |
| Study Type | In Vitro | |
| Model | RF and ELF exposure on DNA and proteins: in vitro and theoretical studies. | |
| Details | Theoretical model outlining possible mechanism of RF and ELF interaction with DNA to produce increases in gene transcription. The authors suggest that EM fields may interact with electrons in DNA so as to destabilize hydrogen (H)-bonds, unzip or loosen the double helix, and make otherwise non-active regions of DNA accessible for transcription. The authors cite their own studies reporting gene expression increases in Na/K ATPase, cytochrome oxidase, c-myc, histone H2B, and the Belousov-Khabotinski reaction and hypothesize effects could exist at external field strengths (for ELF fields) of 10 microT (100 mG) and that a single electron might be displaced by approximately 109 m/sec2. Further, repeated pulses could set up vibrations that destabilize the bonds. Authors' abstract: Lin et al. (1999): HSP70 gene expression is induced by a wide range of environmental stimuli, including 60-Hz electromagnetic fields. In an earlier report we showed that the induction of HSP70 gene expression by magnetic fields is effected at the level of transcription and is mediated through c-myc protein binding at two nCTCTn sequences at -230 and -160. in the human HSP70 promoter. We report on the identification of a third c-myc binding site (between -158 and -162) that is an important regulator of magnetic field-induced HSP70 expression. We also show that the heat shock element (HSE), lying between -180 and -203, is required for induction of HSP70 gene expression by magnetic fields. The HSE centered at -100 alone is insufficient. Authors' abstract: Blank and Goodman (1999): A wide variety of environmental stimuli induce the expression of stress response genes, including high temperatures, hypoxia, heavy metal ions, and amino acid analogs. Stress genes are also induced by low frequency magnetic fields. The cellular response to magnetic fields is activated by unusually weak stimuli, and involves pathways only partially associated with heat shock stress. Since magnetic fields interact with moving charges, as we have shown in enzymes, it is possible that magnetic fields stimulate the stress response by interacting directly with moving electrons in DNA. In this paper, we review several lines of evidence that support this hypothesis. Authors' abstract: Blank and Goodman (2009): Electromagnetic fields (EMF), in both ELF (extremely low frequency) and radio frequency (RF) ranges, activate the cellular stress response, a protective mechanism that induces the expression of stress response genes, e.g., HSP70, and increased levels of stress proteins, e.g., hsp70. The 20 different stress protein families are evolutionarily conserved and act as 'chaperones' in the cell when they 'help' repair and refold damaged proteins and transport them across cell membranes. Induction of the stress response involves activation of DNA, and despite the large difference in energy between ELF and RF, the same cellular pathways respond in both frequency ranges. Specific DNA sequences on the promoter of the HSP70 stress gene are responsive to EMF, and studies with model biochemical systems suggest that EMF could interact directly with electrons in DNA. While low energy EMF interacts with DNA to induce the stress response, increasing EMF energy in the RF range can lead to breaks in DNA strands. It is clear that in order to protect living cells, EMF safety limits must be changed from the current thermal standard, based on energy, to one based on biological responses that occur long before the threshold for thermal changes. AUTHORS' ABSTRACT: Blank and Goodman 2012 (IEEE #6213): We propose a biologically based measure of EMF radiation to replace the energy-based "specific absorption rate" (SAR). A wide range of EMF frequencies has been linked to an increased risk of cancer. The SAR value used to measure the EMF dose and set the safety standard in the radiofrequency (RF) range fails as a standard for predicting cancer risk in the ELF power frequency range. Because cancers are believed to arise from mutations in DNA, changes in DNA induced by interaction with EMF could be a better measure of the biologically effective dose in both frequency ranges. The changes can be measured by transcriptional alterations and/or translational changes in specific proteins. Because ionizing radiation also causes DNA damage, a biologically based standard related to stimulation of DNA could apply over a much wider range of the electromagnetic spectrum. A safety standard for exposure to a wide range of non ionizing frequencies can be based on the documented changes in DNA biochemistry that arise from interactions with EMF. AUTHORS' ABSTRACT: Blank and Goodman 2011 (IEEE #6236): PURPOSE: To review the responses of deoxyribonucleic acid (DNA) to electromagnetic fields (EMF) in different frequency ranges, and characterise the properties of DNA as an antenna. MATERIALS AND METHODS: We examined published reports of increased stress protein levels and DNA strand breaks due to EMF interactions, both of which are indicative of DNA damage. We also considered antenna properties such as electronic conduction within DNA and its compact structure in the nucleus. RESULTS: EMF interactions with DNA are similar over a range of non-ionising frequencies, i.e., extremely low frequency (ELF) and radio frequency (RF) ranges. There are similar effects in the ionising range, but the reactions are more complex. CONCLUSIONS: The wide frequency range of interaction with EMF is the functional characteristic of a fractal antenna, and DNA appears to possess the two structural characteristics of fractal antennas, electronic conduction and self symmetry. These properties contribute to greater reactivity of DNA with EMF in the environment, and the DNA damage could account for increases in cancer epidemiology, as well as variations in the rate of chemical evolution in early geologic history. |
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| Findings | Effects | |
| Status | Completed With Publication | |
| Principal Investigator | Columbia University, USA - rmg5@columbia.edu | |
| Funding Agency | Private/Instit. | |
| Country | UNITED STATES | |
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