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Electromagnetic fields and DNA damage
Abstract
A major concern of the adverse effects of exposure to non-ionizing electromagnetic field (EMF) is cancer induction. Since the majority of cancers are initiated by damage to a cell's genome, studies have been carried out to investigate the effects of electromagnetic fields on DNA and chromosomal structure. Additionally, DNA damage can lead to changes in cellular functions and cell death. Single cell gel electrophoresis, also known as the 'comet assay', has been widely used in EMF research to determine DNA damage, reflected as single-strand breaks, double-strand breaks, and crosslinks. Studies have also been carried out to investigate chromosomal conformational changes and micronucleus formation in cells after exposure to EMF. This review describes the comet assay and its utility to qualitatively and quantitatively assess DNA damage, reviews studies that have investigated DNA strand breaks and other changes in DNA structure, and then discusses important lessons learned from our work in this area.
... Apart from the specifc therapeutic effects when weak static or ELF technical EMFs mimic natural/endogenous EMFs, thousands of studies during the past fve decades have indicated a variety of adverse biological effects induced in a variety of organisms/cell types by exposure to man-made EMFs, especially ELF and complex "RF" (including ELF modulation/pulsation/variability). The recorded biological and health effects range from alterations in the synthesis rates of critical biomolecules such as proteins, RNA, DNA, etc., alterations in enzymatic activity, in intracellular ionic concentrations (Ca +2 , Na + , K + , Cl − , etc.), or in cell proliferation rates, to oxidative stress (OS), DNA and protein damage, chromosome damage, cell death, infertility, electro-hypersensitivity (EHS), and cancer (Marino and Becker 1977;Wertheimer and Leeper 1979;Adey 1981;Goodman et al. 1995;Santini et al. 2005;Diem et al. 2005;Hardell et al. 2007;2013;Phillips et al. 2009;Khurana et al. 2009;Blackman 2009;Johansson 2009;De Iuliis et al. 2009;Yakymenko et al. 2011;Houston et al. 2016;Panagopoulos 2011;2019a;2019b;2020;Panagopoulos et al. 2007a;2007b;2010;2013a;Chavdoula et al. 2010;Miller et al. 2018;Belpomme and Irigaray 2020). All these reported effects are not accompanied by heating of the exposed biological tissues. ...
... Today, there are hundreds of studies that correspond specifc biological effects to specifc incident radiation/feld intensities at different frequency bands which can be measured much more easily and reliably than SAR (see Panagopoulos et al. 2010, andreviews Adey 1981;Goodman et al. 1995;Santini et al. 2005;Phillips et al. 2009;Panagopoulos and Margaritis 2009;Manna and Gosh 2016;Leach et al. 2018;Panagopoulos 2019a). Thus, we can predict the expected effect by knowing the incident radiation/feld intensity plus the other parameters of the feld/exposure (Panagopoulos et al. 2013b). ...
... The same conditions with unequal amplitudes create elliptically polarized felds. Circularly and elliptically polarized 50-60 Hz sinusoidal alternating electric and magnetic felds produced by three-phase electric power transmission lines (120° phase difference among each two phases) are accused for association with cancer, while linearly polarized such felds produced in the lab are repeatedly found to induce DNA damage, cell death, infertility, alterations in DNA synthesis, and cell proliferation rates, and a variety of other adverse effects in experimental animals and cell cultures (Marino and Becker 1977;Wertheimer and Leeper 1979;Adey 1981;Schimmelpfeng and Dertinger 1993;Goodman et al. 1995;IARC 2002;Ivancsits et al. 2002;Santini et al. 2005;Phillips et al. 2009;Panagopoulos et al. 2013a). ...
All types of man-made electromagnetic fields (EMFs) and corresponding non-ionizing electromagnetic radiation (EMR) produced by electric/electronic circuits and antennas – in contrast to natural EMFs/EMR – are totally polarized and coherent. Polarized/coherent EMFs/waves can produce constructive interference and amplify their intensities at certain locations. Moreover, they induce parallel/coherent forced oscillations of charged/polar molecules – especially mobile ions – in living cells/tissues, which can trigger biological effects. The most bioactive man-made EMFs are those employed in wireless communications (WC). They are usually referred to simply as Radio Frequency (RF) or Microwave (MW) EMFs/EMR because they emit carrier signals in the RF/MW band. Yet, WC EMFs contain emissions in the Extremely Low Frequency (ELF), Ultra Low Frequency (ULF), and Very Low Frequency (VLF) bands as well in the form of modulation, pulsing, and variability. This complexity and variability of WC EMFs, combined with polarization, is what makes them even more bioactive. Man-made EMFs (including WC) at environmentally existing intensities do not induce significant heating in living tissues. The Specific Absorption Rate (SAR) was introduced by health agencies as the principal metric for the bioactivity of RF/microwave EMFs. Estimation of SAR from tissue conductivity is inaccurate, and estimation from tissue specific heat is possible only for thermal effects. Thus, SAR is of little relevance, and EMF exposures should better be defined by their incident radiation/field intensity at the included frequency bands, exposure duration, and other field parameters. The present chapter also explains that man-made EMFs/EMR, in contrast to light and ionizing electromagnetic emissions, do not consist of photons but of continuous “classical” waves and, thus, do not obey Planck's formula connecting photon energy (ϵ) with frequency (ν), ϵ = h ν. Apart from polarization, man-made EMFs differ from natural EMFs in frequency bands and emission sources. Basic concepts of interaction with living tissue are discussed.
... Therefore, for in vitro experiments, comparison or reproducibility is a challenge. This is not only due to different experimental settings but can be caused even by slight modifications of the evaluating methods [8,16]. ...
... Carcinogenic growth is mostly initiated by damage to the cell's genome, and therefore, many studies have investigated the effects of electromagnetic fields on DNA and chromosomal structure [16]. ...
... The published experiments studying the effects of radiofrequency radiation differ in the type of investigated cells, frequency and intensity of the electromagnetic radiation, time of exposure, and methods evaluating the effects of exposure on cells and DNA. The most important parameters of the experiments are summarized below [8,[16][17][18][19][20][21][22]: Method ...
The negative influence of non-ionizing electromagnetic radiation on organisms, including humans, has been discussed widely in recent years. This paper deals with the methodology of examining possible harmful effects of mobile phone radiation, focusing on in vivo and in vitro laboratory methods of investigation and evaluation and their main problems and difficulties. Basic experimental parameters are summarized and discussed, and recent large studies are also mentioned. For the laboratory experiments, accurate setting and description of dosimetry are essential; therefore, we give recommendations for the technical parameters of the experiments, especially for a well-defined source of radiation by Software Defined Radio.
... Numerous studies have reported genotoxic effects of both RF/microwave (actually WC) and pure ELF EMFs on a variety of organisms and cell/tissue types (see reviews in Phillips et al. 2009;Panagopoulos 2019bPanagopoulos , 2023Lai 2021;Jagetia 2022). The genetic damage is accompanied by oxidative stress (OS) due to reactive oxygen species (ROS) generation and recent data point that actually genetic damage is due to OS in the cells (Yakymenko et al. 2016;Panagopoulos et al. 2021;Yakymenko and Tsibulin 2022b). ...
... This causes irregular gating, and thus, dysfunction of the VGICs, which leads to intracellular release of ROS that finally cause genetic/cellular damage . This is in line with the attribution of the DNA and chromosome damage to OS by El Abd and Eltoweissy (2012), the confirmed connection of anthropogenic EMF exposures with OS (Phillips et al. 2009;Pall 2013;Yakymenko et al. 2016), and the known effect of ROS on DNA and other cellular macromolecules (Barzilai and Yamamoto 2004). Although certain other studies have reported no connection between simulated WC EMF signals and OS (Poulletier de Gannes et al. 2011), today there is compelling evidence that man-made (including WC) EMF exposures, and mostly real-life exposures, induce a variety of biological/health effects which are in most, if not in all, cases accompanied by OS (Yakymenko et al. 2016;Yakymenko and Tsibulin 2022b). ...
I previously reported chromosomal damage in human peripheral blood lymphocytes (HPBLs) induced by: a) mobile telephony (MT) electromagnetic fields (EMFs)/electromagnetic radiation (EMR), b) a high caffeine dose, and c) the combination of the two stressors. HPBLs from the same subjects exposed to gamma radiation at doses 0.1, 0.3, or 0.5 Gy, displayed more aberrations than those exposed to MT EMFs or the high caffeine dose in a dose-dependent manner. When the cells exposed to these gamma radiation doses were pre-exposed to a single 15-min MT EMF exposure, the number of aberrations increased significantly more than the sum number of aberrations induced by the individual stressors in all subjects. Thus, MT EMF exposure at a power density ~136 times below the latest International Commission on Non-Ionizing Radiation Protection (ICNIRP) exposure limit, apart from the fact that it is genotoxic by itself, significantly enhanced the genotoxic action of gamma radiation. Since gamma radiation at similar doses is applied for diagnostic and therapeutic purposes, people should be aware of the increased risk during treatment periods. Comparison of the genotoxic action between MT EMF and gamma radiation shows that the ICNIRP limits are, at least, ~4.5×10 4 times less stringent than the limits for gamma radiation.
... The frequency of polymorphisms observed in DNA repair mechanism genes in children with acute leukaemia living close to high energy lines reveals the effect of this energy on the repair process. Significant evidence has been reported that genotoxic effects occur in various cell types when exposed to RF-EMF waves (6)(7)(8)(9)(10). Here, it has been reported that cells exposed to RF-EMF waves (1.800 MHz, SAR 2 W/kg) cause oxidative damage in mitochondrial DNA, DNA breaks in neurons and DNA breaks in amniotic cells (6,10). ...
... Here, it has been reported that cells exposed to RF-EMF waves (1.800 MHz, SAR 2 W/kg) cause oxidative damage in mitochondrial DNA, DNA breaks in neurons and DNA breaks in amniotic cells (6,10). Similarly, the damage has been reported in lymphocytes exposed to various RF-EMF waves (8). However, exposure to RF-EMF waves is known to cause chromosome imbalance, changes in gene expression, and gene mutations. ...
Genotoxic Effects of Radiofrequency-Electromagnetic Fields. IntroductionRadiation is energy emission in the form of electromagnetic waves emitted from the solar system and natural resources on earth. The currents produced by the elementary particles formed by the electric current create the magnetic field. Earth's surface is under the influence of the geomagnetic field emanating from the sun. However, the outer liquid also has a magnetic field created as a result of heat transfer in the core. Therefore, all living organisms on earth live under the influence of electromagnetic fields (EMF). Today, besides these natural energy resources, rapidly developing technological developments provide most of the convenience in our lives and expose people to artificial electromagnetic fields. However, man's magnetic field is also under the influence of other natural and artificial magnetic fields around him. In particular, by ionizing radiation, which carries enough energy to break down the genetic material, die cells as a result of DNA damaging, and other diseases, especially cancer, can develop as a result of tissue damage. Electromagnetic Fields in Our LivesToday, apart from natural geomagnetic fields, radiation is emitted from many technological devices. The spectrum of these fields includes many different types of radiation, from subatomic radiation such as gamma and X-rays to radio waves, depending on their wavelengths. Though, as a result of the rapid increase of technological growth, the duration and amount of exposure to EMF is also steadily increasing. On the other hand, wireless gadgets such as computers, smartphones and medical radiological devices have become a necessity for humans. Almost everyone is exposed to radiofrequency electromagnetic fields (RF-EMF) from cell phone and base station antennas or other sources. Thus, the damage caused by the radiation to the environment affects living organisms even many kilometres away unlimitedly. All organisms in the world live under the influence of these negative environmental changes and a large part of the world population is exposed to radiofrequency (RF) radiation for a long time in their daily lives. So, though we are not aware of it, our organs and tissues are constantly exposed to radiation. Therefore, radiation adversely affects human, animal and plant health and disrupts the environment and ecological balance. An example of negative effects, radiation can cause genetic changes in the body (Figure 1). Radiation is divided into ionizing and non-ionizing. Ionizing radiations cause electron loss or gain in an atom or group of atoms in the medium they pass through. Thus, positively or negatively charged ions are formed. High energy X, gamma, ultraviolet and some visible rays in the ionized region of the electromagnetic spectrum can be counted. Since gamma rays, X rays and ultraviolet rays can ionize the molecules in living things more, they can easily disrupt the chemical structure of tissues, cells and DNA molecules in living organisms. Therefore, they can be very dangerous and deadly to living things. The energy of the waves in the non-ionizing region of the electromagnetic spectrum is low and the energy levels are insufficient for the ionization of molecules. Electricity, radio and TV waves, microwaves, and infrared rays are not ionizing because they have low energy. Waves emitted from electronic devices (cell phones, computers, microwave ovens, etc.) are absorbed by the human and animal body. The amount of energy absorbed by the unit biological tissue mass per unit time is called the specific absorption rate (SAR), and its unit is W/kg. Risks of Electromagnetic Fields on Living ThingsDepending on the structure of the tissues and organs, the radiation must reach a certain threshold dose for the effect to occur. Radiation levels below the threshold dose are not effective. Depending on the structure of the tissues and organs, the radiation must reach a certain threshold dose. The effects of small doses of waves are negligible. However, the clinical effects of waves above a certain threshold may increase. High dose waves can cause cell death in tissues. Damages in the cell may increase the risk of cancer and hereditary damage after a while, and somatic effects in people exposed to radiation may cause cancer to appear years later. There is much research on the effects of RF fields. In vitro and in vivo studies on rats, plants and different tissues of humans; suggests that the RF fields are not genotoxic and the fact that harmful effect is due to the heat effect. The contradictory results on this issue have brought about discussions. Therefore, there are still concerns about the potential adverse effects of RFR on human health. A good understanding of the biological effects of RF radiation will protect against potential damages. Due to these uncertainties, with the electromagnetic field project of the World Health Organization, experimental and modelling studies on the biological effects of RF radiation have been accelerated. In 2011, the International Agency for Research on Cancer decided that RF-EMR waves could be potentially carcinogenic to humans (2). Considering that almost everyone, including young children, uses mobile phones in addition to other technological devices, the danger of electromagnetic waves has increased social interest. Genotoxic Effects of EMFIn addition to stimulating apoptosis and changes in ion channels, RF-EMF waves also have a potential effect on genetic material. The radiation absorbed by organisms causes the ionization of target molecules. In particular, biological damage may occur as a result of stimulation/ionization of atoms and disruption of molecular structures while ionizing radiation passes through tissue. As a result of ionization in the cell, electron increases and free electrons cause damage, especially in macromolecules and DNA. Free electrons move directly or indirectly. Free electrons directly affect the phosphodiester or H-bonds of DNA. As a result, the phosphodiester bonds of DNA in the cell are broken, single or double-stranded breakages and chemical toxins increase. DNA double-strand breaks are the most relevant biologic damage induced by ionizing radiation (3,4). There are no cells that are resistant to radiation. The nucleus of the cell and especially the chromosomes in dividing cells are very sensitive to radiation. One of the most important effects of radiation on the cell is to suppress cell growth. In particular, growth is impaired in cells exposed to radiation during cell division (mitosis). Consequently, cells with a high division rate are more sensitive to radiation. DNA damage in somatic cells can lead to cancer development or cell death. Cell death can occur as a result of breaking down DNA because ionizing radiation has enough energy to break down the cell's genetic material. Thus, tissues are damaged and cancer development may be triggered. DNA damage caused by radiation in cells is repaired by metabolic repair processes. If the breaks in DNA as a result of DNA damage caused by radiation in cells are not too large, they can be repaired by metabolic repair processes. Still, errors may occur during this repair. Chromosomes containing different genetic codes and information may also occur. In the cell, the released electrons interact with water molecules, indirectly causing the water to be reactively divided into two parts. Free radicals carry an electron that is not electrically shared in their orbits. Free radicals can cause genetic damage in DNA such as nucleotide changes, double and single-strand breaks. Radiation can cause chromosomes to break, stick together and rearrange. All these changes can lead to mutations or even further, the death of the cell. However, in addition to ionizing radiation, extracellular genotoxic chemicals and intracellular oxidative metabolic residues can also create stress in cells during DNA replication and cell division. Damage may occur during DNA replication under such environmental stress conditions. To date, conflicting results have been reported regarding the genotoxic effects of RF-EMF waves on genetic material. It has been reported that the energy of low EM fields is not sufficient to break the chemical bonds of DNA, but the increase in exposure time is effective on the formation of oxygen radicals and the disruptions in the DNA repair process. The absorption of microwaves can cause significant local warming in cells. For example, an increase in temperature has been observed in cells in culture media exposed to waves of high SAR levels. However, there is evidence that reactive oxygen species are formed in cells indirectly and experimentally exposed to RF-EMF waves. Free oxygen radicals can create nucleotide entries in DNA as well as bind cellular components to DNA bases (5). The frequency of polymorphisms observed in DNA repair mechanism genes in children with acute leukaemia living close to high energy lines reveals the effect of this energy on the repair process. Significant evidence has been reported that genotoxic effects occur in various cell types when exposed to RF-EMF waves (6-10). Here, it has been reported that cells exposed to RF-EMF waves (1.800 MHz, SAR 2 W/kg) cause oxidative damage in mitochondrial DNA, DNA breaks in neurons and DNA breaks in amniotic cells (6,10). Similarly, the damage has been reported in lymphocytes exposed to various RF-EMF waves (8). However, exposure to RF-EMF waves is known to cause chromosome imbalance, changes in gene expression, and gene mutations. Such deleterious genetic effects have also been reported in neurons, blood lymphocytes, sperm, red blood cells, epithelial cells, hematopoietic tissue, lung cells, and bone marrow (1,11,12). It has been found that exposure to RF-EMF radiation also increases chromosome numerical aberrations (6,13). It has also been reported that increased chromosome separation in mouse oocytes exposed to EM and increased DNA fragmentation and apoptosis in fly egg cells (14,15). However, increased DNA breaks have been reported in the blastomeres of embryos of pregnant mice exposed to a frequency of 50 Hz, and a decrease in the number of blastocysts has been reported (16). Genetic damages to sex cells can lead to persistent genetic diseases in subsequent generations. Today, X-ray devices used for medical diagnosis have become one of the largest sources of radiation. These radiological procedures used for diagnosis constitute an important part of ionizing radiation. During these processes, the human body is visibly or invisibly affected by X-rays. As a matter of fact, X-rays have effects of disrupting the structure and biochemical activities of DNA, RNA, proteins and enzymes that are vital in the organism (17). Many studies on this subject have revealed that radiation has suppressive and mutational effects on DNA synthesis. These effects can cause serious damage to the cell as well as DNA and chromosome damage. In a recent study, chromosome damage was investigated in patients with X-ray angiography and personnel working in radiological procedures (18). Our findings showed that the beams used in interventional radiological procedures caused chromosomal damage and the rate of chromosomal abnormalities (CAs) increased significantly in patients after the procedure and this damage increased with the amount of radiation dose. Therefore, the radiation dose to be given to the patient should be chosen carefully. Besides, our findings showed that the frequency of CA is significantly higher in personnel working in radiological procedures. This reveals that interventional cardiologists are exposed to high radiation exposure. For this reason, we can say that the personnel working in radiological procedures (physician, health technician and nurse) are very likely to get diseases after years because they are exposed to low doses but long-term X-rays. Therefore, both the potential risks and safety of exposure to medical radiological devices must be continuously monitored. Furthermore, the fact that chromatid and chromosome breaks are very common among structural CAs in our findings suggests that they may be the cause of malignancy. Because, there are many cancer genes, tumour suppressor genes, enzyme genes involved in DNA repair and important genes or candidate genes responsible forapoptosis on these chromosomes. All this information shows that patients are more susceptible to DNA damage and inappropriate radiological examinations should be avoided. Therefore, X-ray and other diagnostic imaging techniques should not be applied unless necessary, and physicians and patients should be more careful in this regard. It has been reported that RF-EMR waves emitted from wireless communication device mobile phones have a genotoxic effect on human and mammalian cells (6,19). In a recent study; The effects of 900 and 1800 MHz cell phone frequencies on human chromosomes were investigated in amniotic cell cultures (6). Here, it has been reported that chromosome packing delays, damage and breaks occur in amniotic cells exposed to 900 and 1800 MHz every day at 3, 6 and 12 hours for twelve days. However, it was found that the frequency of 1800 MHz caused more CAs than 900 MHz, and the amount of damage increased with increasing usage time. These results confirm that GSM-like RF-EMR causes direct genotoxic effects in human in vitro cultures and has adverse effects on human chromosomes, and these effects increase in parallel with exposure time. This shows us that the mobile phone carries a risk for human health and these genetic damages can cause cancer. Therefore, necessary precautions should be taken for these harmful effects of mobile phones. Among these measures, the periods of mobile phone use should be kept short, especially the exposure of developing children and infants to mobile phones should be prevented, and avoiding excessive use of mobile phones may be one of the precautions against cancer. However, in order to evaluate it in more detail, the effects of mobile phones with environmental mutagens and/or carcinogens should be considered in subsequent researches. Conclusion
Today, in parallel with the increasing technological developments, the demand of the society for electronic devices and phones and the frequency ranges of electronic devices are constantly increasing. Waves emitted from electronic devices are absorbed by human and animal bodies. Especially, the use of phones by contact with our body and the increase in usage time affects not only adults but also young children. Therefore, there is increasing concern in society about the negative biological effects of EM waves emitted from phones and other electronic devices. Results from all studies show that RF-EMF waves may be carcinogenic due to their genotoxic effect. Because cancer is a disease that occurs as a result of genetic damage. Considering these negative and harmful effects, regulations following international standards regarding the use of electronic devices should be made and society should be made aware of the risks.References Kim JH.; Lee K.; Kim HG.; Kim KB.; Kim HR. Possible Effects of Radiofrequency Electromagnetic Field Exposure on Central Nerve System. Biomol Ther. 2019, 27(3), 265-275. Baan R.; Grosse Y.; Lauby-Secretan B.; et al. WHO International Agency for Research on Cancer Monograph Working Group. Carcinogenicity of radiofrequency electromagnetic fields. Lancet Oncol. 2011, 12, 624–626. Berrington De Gonzalez A.; Darby S. Risk of cancer from diagnostic X-rays: estimates for the UK and 14 other countries. Lancet. 2004, 363, 345-351. Löbrich M.; Jeggo PA.The impact of a negligent G2/M checkpoint on genomic instability and cancer induction. Nat Rev Cancer. 2007, 861–869. M Valko.; M Izakovic.; M Mazur.; CJ Rhodes.; J Telser. Role of oxygen radicals in DNA damage and cancer incidence. Cell. Biochem. 2004, 266, 37–56. Uslu N.; Demirhan O.; Emre M.; Seydaoğlu G. The chromosomal effects of GSM-like electromagnetic radiation exposure on human fetal cells. Biomed Res Clin Prac. 2019, 4, 1-6. Lee S.; Johnson D.; Dunbar K Dong H.; Ge X.; Kim YC.; Wing C.; Jayathilaka N.; Emmanuel N.; Zhou CQ.; Gerber HL.; Tseng CC.; Wang SM. 2.45 GHz radiofrequency fields alter gene expression in cultured human cells. FEBS Lett. 2005, 579, 4829-4836. Phillips JL.; Singh NP.; Lai, H. Electromagnetic fields and DNA damage. Pathophysiology. 2009, 16, 79-88. Ruediger HW. Genotoxic effects of radiofrequency electromagnetic fields. Pathophysiology. 2009, 16, 89-102. Xu S.; Zhou Z.; Zhang L.; Yu Z.; Zhang W.; Wang Y.; Wang X.; Li M.; Chen Y.; Chen C.; He M.; Zhang G.; Zhong M. Exposure to 1800 MHz radiofrequency radiation induces oxidative damage to mitochondrial DNA in primary cultured neurons. Brain Res. 2010, 1311, 189-196. Demsia G.; Vlastos D.; Matthopoulos DP. Effect of 910-MHz electromagnetic field on rat bone marrow. 2004, 2, 48-54. Zhao TY.; Zou SP.; Knapp PE. Exposure to cell phone radiation up-regulates apoptosis genes in primary cultures of neurons and astrocytes. Lett. 2007, 412, 34-38. Mashevich M.; Folkman D.; Kesar A.; Barbul A.; Korenstein R.; Jerby E.; Avivi L. Exposure of human peripheral blood lymphocytes to electromagnetic fields associated with cellular phones leads to chromosomal instability. Bioelectromagnetics. 2003, 24, 82-90. Panagopoulos DJ.; Chavdoula ED.; Nezis IP.; Margaritis LH. Cell death induced by GSM 900-MHz and DCS 1800-MHz mobile telephony radiation. Mutat Res. 2007, 626(1–2), 69–78. Sagioglou NE.; Manta AK.; Giannarakis IK.; Skouroliakou AS.; Margaritis LH. Apoptotic cell death during Drosophila oogenesis is differentially increased by electromagnetic radiation depending on modulation, intensity and duration of exposure. Electromagn Biol Med. 2015, 1-14. Borhani N.; Rajaei F.; Salehi Z.; Javadi A. Analysis of DNA fragmentation in mouse embryos exposed to an extremely low-frequency electromagnetic field. Electromagn Biol Med. 2011, 30(4), 246–252. Rowley R.; Phillips EN.; Schroeder AL. Effects of ionizing radiation on DNA synthesis in eukaryotic cells. Int J Radiat Biol. 1999, 75( 3), 267-283. Çetinel N.; Demirhan O.; Demirtaş M.; Çağlıyan ÇE.; Cüreoğlu A.; Uslu IN.; Sertdemir Y. The Genotoxic Effect Of Interventional Cardiac Radiologic Procedures On Human Chromosomes. Clinical Medical Reviews and Reports. 2020, 3(1), 1-10. Aitken RJ.; Bennetts LE.; Sawyer D.; Wiklendt AM.; King BV. Impact of radio frequency electromagnetic radiation on DNA integrity in the male germline. Int J Androl. 2005, 28(3), 171–179.
... In critical sectors such as defense and healthcare, where reliability is paramount, EMI can pose severe operational challenges, highlighting the need for robust shielding solutions. High-frequency EM energy may disrupt and resonate with DNA and other biological activities, potentially triggering malignant alterations [4], [5]. Prolonged exposure to electromagnetic waves (EMWs) has been linked to a range of health issues, including anxiety, fatigue, brain tumors, insomnia, nervousness, and leukemia [6]- [9]. ...
The surge in electronic devices and wireless communication technologies has increased the demand for effective electromagnetic interference shielding and microwave-absorbing materials. Traditional electromagnetic interference (EMI) shielding materials, which predominantly utilize metals and polymer composites, pose significant environmental challenges due to their non-biodegradable nature. Recently, a range of novel electromagnetic shielding materials has been developed, with composite materials derived from waste sources emerging as promising alternatives for next-generation shielding solutions. This comprehensive review explores sustainable materials derived from various recycled waste sources for EMI shielding applications. It begins by examining the fundamental principles and mechanisms of EMI shielding and absorption techniques necessary for cost-effective performance. The review further investigates a variety of sustainable materials, including agricultural residues, industrial by-products, animal waste, and electronic waste, evaluating their potential for EMI shielding. Additionally, it explores the structural characteristics, electromagnetic properties, and synthesis methods of composite materials created from different raw material combinations. The review highlights the processing techniques and integration strategies used to develop effective shielding materials, as well as the potential applications of these materials and the challenges associated with their synthesis. The innovative use of solid waste materials from diverse origins in creating these shielding materials not only enhances their efficiency but also contributes to effective waste management and environmental sustainability.
... The biological effects of nonionizing RF-EMR have drawn considerable scientific scrutiny during the past two decades (Havas 2017). The epidemiological studies were complemented by in-vivo and in-vitro studies that explored the biological effects of electromagnetic fields (Phillips et al. 2009). Among the biological effects elicited by RF-EMR exposure, the onset of oxidative stress, cell death, reproductive decline and even cancer induction were shown in most of the studies conducted on both mammalian and non-mammalian species (Panagopoulos 2019;Piccinetti et al. 2018). ...
Biological effects of radio frequency electromagnetic radiation (RF-EMR) in the range of 900-1800 MHz emerging from the mobile phone were investigated and were found to influence the locomotor pattern when exposure was initiated from 1 hour post fertilization (hpf) in zebrafish embryos (ZE), Danio rerio. Mobile phones and other wireless devices offer tremendous advantages. However, on the flipside they are leading to an increased electromagnetic energy in the environment, an excess of which could be termed as electromagnetic pollution. Herein, we tried to understand the effects of RF-EMR emerging from the mobile phone, on the development and behavior of ZE, exposed to RF-EMR (specific absorption rate of 1.13 W/kg and 1800 MHz frequency) 1 hr daily, for 5 days. To understand if there could be any developmental stage-specific vulnerability to RF-EMR, the exposure was initiated at three different time points: 1hpf, 6hpf and 24hpf of ZE development. Observations revealed no significant changes in the survival rate, morphology, oxidative stress or cortisol levels. However, statistically significant variations were observed in the batch where exposure started at 1hpf, with respect to locomotion patterns (distance travelled: 659.1 ± 173.1 mm Vs 963.5 ± 200.4 mm), which could be correlated to anxiety-like behavior; along with a corresponding increase in yolk consumption (yolk sac area: 0.251 ± 0.019 mm2 Vs 0.225 ± 0.018 mm2). Therefore, we conclude that RF-EMR exposure influences the organism maximally during the earliest stage of development, and we also believe that an increase in the time of exposure (corresponding to the patterns of current usage of mobile phones) might reveal added afflictions.
... Studies have shown that RFR can have a negative effect on the brain (Hidisoglu et al., 2016;Megha et al., 2012). Moreover, RFR has been reported to increase resting blood pressure, reduce melatonin production, increase DNA chain breaks, chromosomal instability, and increased risk of cancer (Dyche et al., 2012;Phillips et al., 2009;Szmigielski et al., 1998). Recently, many studies have been carried out on the effect of RFR on male infertility (Al-Damegh, 2012;Dasdag et al., 2003;Guo et al., 2019). ...
With advances in technology, the emission of radiofrequency radiation (RFR) into the environment, particularly from mobile devices, has become a growing concern. Tyro 3, Axl, and Mer (TAM) receptors and their ligands are essential for spermatogenesis and testosterone production. RFR has been shown to induce testicular cell apoptosis by causing inflammation and disrupting homeostasis. This study aimed to investigate the role of TAM receptors and ligands in the maintenance of homeostasis and elimination of apoptotic cells in the testes (weeks), short-term sham exposure (sham/1 week), and middle-term sham exposure (sham/10 weeks). Testicular morphology was assessed using hematoxylin-eosin staining, while immunohistochemical staining was performed to assess expression levels of TAM receptors and ligands in the testes of all groups. The results showed that testicular morphology was normal in the control, sham/1 week, and sham/10 weeks groups. However, abnormal processes of spermatogenesis and seminiferous tubule morphology were observed in RFR exposure groups. Cleaved Caspase 3 immunoreactivity showed statistically significant difference in 1 and 10 weeks exposure groups compared to control group. Moreover, there was no significant difference in the immunoreactivity of Tyro 3, Axl, Mer, Gas 6, and Pros 1 between groups. Moreover, Tyro 3 expression in Sertoli cells was statistically significantly increased in RFR exposure groups compared to the control. Taken together, the results suggest that RFR exposure negatively affects TAM signalling, preventing the clearance of apoptotic cells, and this process may lead to infection and inflammation. As a result, rat testicular morphology and function may be impaired.
... The frequency ranges that are applied to modern electrical technologies that concern human and animal health are in general, Extremely Low Frequency (ELF) 3 Hz -30 Hz, Super Low Frequency (SLF) 30 Hz -300 Hz (power lines, household electrical appliances, computers, etc) and Ultra High Frequency (UHF) 300 MHz -3 GHz (digital television, mobile phones, routers, etc). It should be noted that long-term exposure to electromagnetic field (EMF), even of minor strength, may influence people's well-being [1][2][3][4][5][6][7][8][9]. ...
The aim of this paper was to establish whether electromagnetic fields (EMF) with a super lowfrequency (SLF) have a negative effect on onion seed quality. Three sectors were separated on the deviceemitting electromagnetic fields: „E” – sector emitting electromagnetic radiation with the predominance of theelectrical component, „EM” – sector emitting electromagnetic radiation without domination of its componentsand „M” – sector with a predominance of magnetic component. Seed germination and vigour were evaluatedat 20 oC in darkness. Mycological analysis was performed using a agar plate method. Exposure of seeds toelectromagnetic fields did not affect Gmax. Treated seeds were characterized with significantly lowergermination capacity and higher percentage of deformed abnormal seedlings than untreated seeds. Electro-magnetic radiation with the predominance of electrical component (E), and electromagnetic radiation with thepredominance of magnetic component (M) also significantly decreased the germination energy. The effect ofelectromagnetic fields on the speed of germination was ambiguous. Seeds treated with the electromagneticfield with predominance of magnetic component (M), and electromagnetic field without domination of itscomponents (EM) germinated significantly less uniformly than control. Generally, exposure of seeds toelectromagnetic fields did not influence the incidence of fungi.
... These deviations result in some unwanted events such as disabilities, damages in tissues and organs, and genetic diseases. 6,7 Some technological devices such as cell phone, which have been ever increasingly produced and used in recent years, result in electro-magnetic pollution by producing electro-magnetic waves. The observations and studies carried out up until now indicate that electro-magnetic waves may increase the frequency of brain cancer formation. ...
Objective: There is current news that emerges regarding the relationship between the magnetic effects of cell phones and some types of cancer. In spite of the studies carried out, the level of evidence of this news is low, and also the relationship between the magnetic effects of cell phones and other types of cancer is not certain except for brain cancer. In this study, it is aimed at examining the effects of magnetic field of cell phones on the samples of breast cancer human myeloid leukemia cell growth. Methods: In the study, breast cancer MCF-7 and leukemia K562 cell lines were used as the source of cancer cell. During the six-day cell culture, cancer cells were subjected to the effects of cell phone by using a telephone call program (Automated outbound call software). The system made 6 calls for 1 minute for each call once in 144 minutes from fixed line. The number of cultured cells and proliferation capacities of the two types of tumor cells in the control and experimental groups were assessed. Results: The number of cancer cells, which were subjected to the effects of cell phone as a result of the culture of tumor cells, was found lower when compared with control group (7500000 ± 100000 vs 6625000 ± 225000 for MCF-7; 15412500 ± 112500 vs 13700000 ± 250000 for K562; P < 0.05 for both). In MTT test, it was found out that two types of cell proliferation was inclined to slow down with the effect of cell phone. Conclusion: The results can be translated that cell phone may inhibit neoplastic transformation, and this observation may promote to initiate a new clinical studies both for healthy people and for patients with cancer.
... However, a large and long-term study on mice showed that short-and long-term exposure to ELF-MF did not elevate the markers of oxidative stress [64]. Another theory suggested that exposure to magnetic fields results in DNA strand breaks in the brain cells and this may cause apoptosis and necrosis [65]. Nevertheless, this is not consistently supported by animal studies [66]. ...
Exposure to extremely low frequency magnetic fields (ELF-MF) and electric shocks occurs in many workplaces and occupations but it is unclear whether any of these exposures cause Amyotrophic lateral sclerosis (ALS). The aim of this systematic review and meta-analysis is to explore whether occupational exposure to ELF-MF and/or electric shocks are risk factor for ALS. We searched PubMed, Embase, and Web of Science databases up to the end of 2019. Pooled risk estimates were calculated using random-effects meta-analysis including exploration of the sources of heterogeneity between studies and publication bias. Twenty-seven publications fulfilled the inclusion criteria. We found a weak, significant, association between occupational exposure to ELF-MF and the risk of ALS (RR Pooled estimate : 1.20; 95%CI: 1.05, 1.38) with moderate to high heterogeneity (I 2 =66.3%) and indication of publication bias (P Egger's test =0.03). No association was observed between occupational exposure to electric shocks and risk of ALS (RR Pooled estimate : 0.97; 95%CI: 0.80, 1.17) with high heterogeneity (I 2 =80.5%), and little indication for publication bias (P Egger's test =0.24). The findings indicate that occupational exposure to ELF-MF, but not electric shocks, might be a risk factor for ALS. However, given the moderate to high heterogeneity and potential publication bias, the results should be interpreted with caution.
... Therefore, everyone is exposed to a complex mix of weak electric and magnetic fields, both at home and at work [1]. While the health impacts of this form of radiation are inconclusive [2][3][4], many people are concerned about how long-term exposure to excessive EMR may impact human health and nature. As a result, a need to develop textile products that implement electromagnetic shielding has occurred [5]. ...
The aim of this study is to investigate the influence of knitting structure and metal wire amount on the electromagnetic shielding effectiveness (EMSE) of knitted fabrics comparatively. Single jersey, single pique, weft locknit, and cross miss fabrics involving stainless steel or copper wires were produced on a flat knitting machine. A free space measurement technique was used for the EMSE measurements in an anechoic chamber. The variance analysis results of the EMSE values reveal that the effect of knitting structure, metal wire type, metal wire amount, and incident wave frequency is highly significant. It was observed that fabrics with tuck and miss loop structures had higher EMSE values than single jersey fabrics. It was found that single pique fabrics had higher EMSE values than single jersey fabrics that contain twice as much metal wire. It indicates that changing the knitting structure is more effective than changing the metal wire amount.
... There are many reports concerning genotoxic impacts in cellular RFR studies but only some of them involve the cellular immune system with the positive data indicating significant alterations in the immune cells (Aly et al., 2008;Tiwari and Singh, 2012). The exogenous and endogenous stimuli usually damage the DNA, and DNA repair enzymes then perform their function by repairing the damage (Phillips et al., 2009) (Vamvakas et al., 1997). The increase in DNA damage resulted in genetic instability further leading to severe diseases, e.g. ...
Growing evidence recommends that radiofrequency radiations might be a new type of environmental pollutant. The consequences of RFR on the human immune system have gained considerable interest in recent years, not only to examine probable negative effects on health but also to understand if RFR can modulate the immune response positively. Although several studies have been published on the immune effects of RFR but no satisfactory agreement has been reached. Hence this review aims to evaluate the RFR modulating impacts on particular immune cells contributing to various innate or adaptive immune responses. In view of existing pieces of evidence, we have suggested an intracellular signaling cascade responsible for RFR action. The bio-effects of RFR on immune cell morphology, viability, proliferation, genome integrity, and immune functions such as ROS, cytokine secretion, phagocytosis, apoptosis, etc. are discussed. The majority of existing evidence point toward the possible shifts in the activity, number, and/or function of immunocompetent cells, but the outcome of several studies is still contradictory and needs further studies to reach a conclusion. Also, the direct association of experimental studies to human risks might not be helpful as exposure parameters vary in real life. On the basis of recent available literature, we suggest that special experiments should be designed to test each particular signal utilized in communication technologies to rule out the hypothesis that longer exposure to RFR emitting devices would affect the immunity by inducing genotoxic effects in human immune cells.
... However, the BioInitiative working group, together with other researchers [8,10,[12][13][14][15][16], suggest that adverse health effects are observed at low levels of exposure 0.1 µ W/cm 2 . Studies suggest that RF-EMF exposures with powers below the recommendations of the ICNIRP have effects related to changes in brain activity [17], affecting cognitive and motor performance [12,13], infertility problems in the male reproductive system [18,19], DNA damage [20,21], association to different brain tumors and intensity of RF-EMF, and having a greater effect in children and teenagers than in adults [4,6,12,[22][23][24][25]. These studies suggest that exposure to RF-EMF is an important factor to consider as a "possible carcinogen" classified in group 2B by the International Agency for Research on Cancer (IARC) [26]. ...
A novel compact device with spectrum analyzer characteristics has been designed, which allows the measuring of the maximum power received in multiple narrow frequency bands of 300 kHz, recording the entire spectrum from 78 MHz to 6 GHz; the device is capable of measuring the entire communications spectrum and detecting multiple sources of electromagnetic fields using the same communications band. The proposed device permits the evaluation of the cross-talk effect that, in conventional exposimeters, generates a mistake estimation of electromagnetic fields. The device was calibrated in an anechoic chamber for far-fields and was validated against a portable spectrum analyzer in a residential area. A strong correlation between the two devices with a confidence higher than 95% was obtained; indicating that the device could be considered as an important tool for electromagnetic field studies.
... •− (which can be generated either by the plasma membrane NOX or by O 2 after the uptake of single electrons that have been leaked during oxidative phosphorylation). In turn, H 2 O 2 can be converted to • OH by free Fe 2+ (or Cu + ) via the Fenton reaction (Table 1, reaction 1), and its association with the cell's response to EMF in relation to DNA damage has been also suggested [37]. To sustain the production of • OH, Fe 2+ (and Cu + ) must be regenerated via reduction by O 2 ...
Electromagnetic fields (EMFs) disrupt the electrochemical balance of biological membranes, thereby causing abnormal cation movement and deterioration of the function of membrane voltage-gated ion channels. These can trigger an increase of oxidative stress (OS) and the impairment of all cellular functions, including DNA damage and subsequent carcinogenesis. In this review we focus on the main mechanisms of OS generation by EMF-sensitized NADPH oxidase (NOX), the involved OS biochemistry, and the associated key biological effects.
... Temporary heart arrhythmia and muscle contraction are due to the gradient fields and increase in the tissue temperature can be induced by RF field (5). Several in vivo and in vitro investigations have evaluated the biological effects of the three magnetic fields on the human and animal cells and bodies, which were not associated with genetic damages (6)(7)(8). Some studies have reported that MRI may affect genomic DNA in the in vitro conditions (9-11-). ...
Introduction: Magnetic Resonance Imaging (MRI) is a non-invasive imaging modality. However, the effects of MRI on the immune system in the in vivo conditions are yet to be clarified. In this study we explored the effects of routine brain MRI on the protein and mRNA peripheral blood levels of interleukin-6 (IL-6), IL-10, IL-17A and transforming growth factor-beta (TGF-β).
Material and methods: 40 subjects, who referred for brain MRI, were entered for evaluating effects of routine brain MRI on the protein and mRNA peripheral blood levels of IL-6, IL-10, IL-17A and TGF-β. Accordingly, peripheral blood were collected before and 3 hours after MRI from the participants. Protein levels of the cytokines were evaluated using ELISA. Also, mRNA levels were analyzed using Real-Time PCR techniques.
Results: Brain MRI without contrast led to an increase in protein levels of IL-6 in the peripheral serum, but did not change protein and mRNA levels of IL-10, IL-17A and TGF-β. IL-6 mRNA levels after MRI were higher in the participants with mild anxiety compared to those without anxiety.
Conclusion: brain MRI without contrast can induce secretion of IL-6 and may be associated with its functions, such as development of plasma cells or induction of inflammation.
... The mechanisms by which radiofrequency radiation affects cells, tissues, and organisms are not well understood and may include diverse processes such as inhibition of the mitotic spindle apparatus leading to impaired cell division and cell death [22], changes in the activity of voltage-gated calcium channels [23][24][25][26], changes in the concentrations of reactive oxygen species and redox homeostasis [25,[27][28][29][30][31][32], changes in intracellular enzymes and gene expression [33], and changes in membrane permeability [34]. DNA damage following exposure to RFR [35,36] may be a direct effect or due to secondary mechanisms, such as interference with DNA repair processes [37]. As summarized in a recent review, these biological effects of RFR occur without substantial temperature increases in tissues [27]. ...
Background
Epidemiological studies and research on laboratory animals link radiofrequency radiation (RFR) with impacts on the heart, brain, and other organs. Data from the large-scale animal studies conducted by the U.S. National Toxicology Program (NTP) and the Ramazzini Institute support the need for updated health-based guidelines for general population RFR exposure.
Objectives
The development of RFR exposure limits expressed in whole-body Specific Absorption Rate (SAR), a metric of RFR energy absorbed by biological tissues.
Methods
Using frequentist and Bayesian averaging modeling of non-neoplastic lesion incidence data from the NTP study, we calculated the benchmark doses (BMD) that elicited a 10% response above background (BMD 10 ) and the lower confidence limits on the BMD at 10% extra risk (BMDL 10 ). Incidence data for individual neoplasms and combined tumor incidence were modeled for 5% and 10% response above background.
Results
Cardiomyopathy and increased risk of neoplasms in male rats were the most sensitive health outcomes following RFR exposures at 900 MHz frequency with Code Division Multiple Access (CDMA) and Global System for Mobile Communications (GSM) modulations. BMDL 10 for all sites cardiomyopathy in male rats following 19 weeks of exposure, calculated with Bayesian model averaging, corresponded to 0.27–0.42 W/kg whole-body SAR for CDMA and 0.20–0.29 W/kg for GSM modulation. BMDL 10 for right ventricle cardiomyopathy in female rats following 2 years of exposure corresponded to 2.7–5.16 W/kg whole-body SAR for CDMA and 1.91–2.18 W/kg for GSM modulation. For multi-site tumor modeling using the multistage cancer model with a 5% extra risk, BMDL 5 in male rats corresponded to 0.31 W/kg for CDMA and 0.21 W/kg for GSM modulation.
Conclusion
BMDL 10 range of 0.2—0.4 W/kg for all sites cardiomyopathy in male rats was selected as a point of departure. Applying two ten-fold safety factors for interspecies and intraspecies variability, we derived a whole-body SAR limit of 2 to 4 mW/kg, an exposure level that is 20–40-fold lower than the legally permissible level of 0.08 W/kg for whole-body SAR under the current U.S. regulations. Use of an additional ten-fold children’s health safety factor points to a whole-body SAR limit of 0.2–0.4 mW/kg for young children.
... Simultaneously, public concern over the adverse health effects of RF-EMF is escalating. Many prior studies have evaluated the harmful effects of EMFs on human health, including functional cell damage [4], genetic damage, neurological diseases, reproductive disorders, immune disorders, kidney damage, electromagnetic hypersensitivity, and leukemia [5][6][7][8][9][10]. However, these studies have been criticized for methodological limitations, unrealistic exposure levels of RF-EMF, or lack of in vivo evidence to substantiate the in vitro findings related to the hazards of RF-EMF [11]. ...
With the rapid growth of the wireless communication industry, humans are extensively exposed to electromagnetic fields (EMF) comprised of radiofrequency (RF). The skin is considered the primary target of EMFs given its outermost location. Recent evidence suggests that extremely low frequency (ELF)-EMF can improve the efficacy of DNA repair in human cell-lines. However, the effects of EMF-RF on DNA damage remain unknown. Here, we investigated the impact of EMF-long term evolution (LTE, 1.762 GHz, 8 W/kg) irradiation on DNA double-strand break (DSB) using the murine melanoma cell line B16 and the human keratinocyte cell line HaCaT. EMF-LTE exposure alone did not affect cell viability or induce apoptosis or necrosis. In addition, DNA DSB damage, as determined by the neutral comet assay, was not induced by EMF-LTE irradiation. Of note, EMF-LTE exposure can attenuate the DNA DSB damage induced by physical and chemical DNA damaging agents (such as ionizing radiation (IR, 10 Gy) in HaCaT and B16 cells and bleomycin (BLM, 3 μM) in HaCaT cells and a human melanoma cell line MNT-1), suggesting that EMF-LTE promotes the repair of DNA DSB damage. The protective effect of EMF-LTE against DNA damage was further confirmed by attenuation of the DNA damage marker γ-H2AX after exposure to EMF-LTE in HaCaT and B16 cells. Most importantly, irradiation of EMF-LTE (1.76 GHz, 6 W/kg, 8 h/day) on mice in vivo for 4 weeks reduced the γ-H2AX level in the skin tissue, further supporting the protective effects of EMF-LTE against DNA DSB damage. Furthermore, p53, the master tumor-suppressor gene, was commonly upregulated by EMF-LTE irradiation in B16 and HaCaT cells. This finding suggests that p53 plays a role in the protective effect of EMF-LTE against DNA DSBs. Collectively, these results demonstrated that EMF-LTE might have a protective effect against DNA DSB damage in the skin, although further studies are necessary to understand its impact on human health.
... This strongly suggests that the destructive effect of MWs on DNA was not solely related to the temperature increase above the denaturation threshold of 94°C. Several studies further revealed that MWs could affect DNA integrity in different ways, such as single-and double-strand breaks produced by free radicals (Phillips et al. 2009), and could accelerate chemical reactions to result in greater DNA destruction in a shorter time (Yang and Hang 2013). ...
Two 915-MHz microwave treatments (2 kW-8 min and 4 kW-4 min) were applied to soil and their effects were monitored just after treatments (T0) and 26 days (T26) in soil microcosms. Densities of culturable bacteria, fluorescent pseudomonads and nematodes, hydrolysis activity and soil DNA content declined by over 50% immediately after both microwave treatments (T0), excluding the total fungal 18S rRNA (−13 or −17%) and bacterial 16S rRNA copies (non-significant). A rapid shift in bacterial community composition occurred from T0 towards a large increase in the relative abundance of Firmicutes (+1650%) and a concomitant decrease in various phyla (e.g. Acidobacteria, Actinobacteria, Bacteroidetes, Proteobacteria) from −85 to −61%. At T26 and for both treatments, fluorescein diacetate hydrolysis, density of culturable bacteria, 18S rRNA gene numbers, Simpson diversity, relative abundances of Bacteroidetes and Proteobacteria regained levels similar to controls. Alpha, Delta and Gamma classes Proteobacteria also end up reaching a similar level. In contrast, fluorescent pseudomonad density, nematode diversity and abundance, soil DNA content and relative abundances of some phylum (Acidobacteria, Actinobacteria, Chloroflexi) did not increase in such proportions. Most of the soil biological properties have not been permanently impacted. Nevertheless, the recovery kinetics highly differed according properties, with resilience indices at T26 varying from −87 to +99%.
... the exposed electrical field, the frequency, and the span between D. melanogaster and the antenna. Studies have shown that EMR can induce various types of cancer and can cause DNA damage (Brainard et al. 1999;Hardell and Sage 2008;Phillips et al. 2009). In addition, there are experimental studies in the production of ROS which have shown no significant results in apoptosis (Hou et al. 2015). ...
With the development of today’s technology, the electromagnetic radiation spread by mobile phones and base stations is also rapidly increasing, and this causes serious concerns about the environment and human health. The Drosophila model organism is widely used in genetic toxicology studies because its genome is highly similar to the genes identified in human diseases. In this study, the genotoxic effects of radiofrequency electromagnetic radiation were evaluated by the wing Somatic Mutation and Recombination Test (SMART) in Drosophila melanogaster at 900 MHz, 1800 MHz, and 2100 MHz. The SMART method is based on the observation of genetic changes occurring in the trichomes of the Drosophila wings appearing as mutant clones under the microscope. Throughout the study, total clone parameters were evaluated by exposing the Drosophila larvae to electromagnetic fields for two, four, and six hours per day for two days. As a result of the study, it was observed that the number of mutant clones was statistically increased according to the negative control group in all applications except for the six-hour application at 1800 MHz.
... According to previous studies, EMFs may have effects on several cell functions, including cell migration, differentiation, death, and cell stress [8]. In addition, exposure to electromagnetic waves has been reported to be associated with many harmful effects, such as genetic damage, neurological diseases, reproductive disorders, immune disorders, kidney damage, electromagnetic hypersensitivity, and leukemia [9][10][11][12][13][14]. The skin is a barrier of the body against various external harmful factors. ...
With the rapid growth of wireless communication devices, the influences of electromagnetic fields (EMF) on human health are gathering increasing attention. Since the skin is the largest organ of the body and is located at the outermost layer, it is considered a major target for the health effects of EMF. Skin pigmentation represents one of the most frequent symptoms caused by various non-ionizing radiations, including ultraviolet radiation, blue light, infrared, and extremely low frequency (ELF). Here, we investigated the effects of EMFs with long-term evolution (LTE, 1.762 GHz) and 5G (28 GHz) bandwidth on skin pigmentation in vitro. Murine and Human melanoma cells (B16F10 and MNT-1) were exposed to either LTE or 5G for 4 h per day, which is considered the upper bound of average smartphone use time. It was shown that neither LTE nor 5G exposure induced significant effects on cell viability or pigmentation. The dendrites of MNT-1 were neither lengthened nor regressed after EMF exposure. Skin pigmentation effects of EMFs were further examined in the human keratinocyte cell line (MNT-1-HaCaT) co-culture system, which confirmed the absence of significant hyper-pigmentation effects of LTE and 5G EMFs. Lastly, MelanoDerm™, a 3D pigmented human epidermis model, was irradiated with LTE (1.762 GHz) or 5G (28 GHz), and image analysis and special staining were performed. No changes in the brightness of MelanoDerm™ tissues were observed in LTE- or 5G-exposed tissues, except for only minimal changes in the size of melanocytes. Collectively, these results imply that exposure to LTE and 5G EMFs may not affect melanin synthesis or skin pigmentation under normal smartphone use condition.
... There are short-term and long-term effects from phone radiation. The earliest effects are snooze diseases, headaches, gloominess, etc., while long-time effects can be brain tumours, cancer, DNA corruption, memory weakness, etc. (Figure 2) [7]. Cancer is one of the most common diseases in the world, with no specific treatment, so, often studies avoid dealing with it. ...
In this paper, the emitted electromagnetic waves (EMW) from different cellular mobile base stations (BSs) have been measured and calculated in order to study their effects on public health. Moreover, a comparison between the effect of radiated power from the BSs on people who live near them and those who live away has been made by using OpenSignal software and calculated theoretically. The values of power density for different cells were also calculated to compare them with the maximum permissible exposure limit-the acceptable range values of power density. The measurements were done in Tikrit City considering ten cells and various locations and distances. The results show that most of the power density and EMV for the tested cells are within the acceptable range. However, power density and EMV for two of tested cells have hurtful effects in the long term for people who live near the BSs.
... The disruption of cell electrochemical balance by manmade (polarized) EMFs through irregular gating of voltagegated ion channels on cell membranes is described by the "ion forced-oscillation mechanism" (Panagopoulos et al. 2000(Panagopoulos et al. , 2002(Panagopoulos et al. , 2015b(Panagopoulos et al. , 2020. This may lead to DNA damage by intracellular release of free radicals or hydrolytic enzymes like DNases (Barzilai and Yamamoto 2004;Phillips et al. 2009;Panagopoulos 2011;Pall 2013;Yakymenko et al. 2016). This is in line with the attribution of the DNA and chromosome damage to oxidative stress by El Abd and Eltoweissy (2012). ...
I recently reported induction of chromatid-type aberrations in human peripheral blood lymphocytes after a single 15 min exposure to Universal Mobile Telecommunications System (UMTS) Mobile Telephony (MT) electromagnetic field (EMF) from a mobile phone. Lymphocytes from six healthy subjects were stimulated for mitosis, and exposed during the G2/M phase at 1 cm distance from the handset during an active phone call in “talk” mode (Panagopoulos 2019a). The same type of cells from the same subjects treated with a high caffeine dose (~290 times above the permissible single dose for an adult human) exhibited the same type of aberrations in a little smaller but comparable degree. The combination of this caffeine dose and the 15 min MT EMF exposure increased dramatically the number of aberrations in all subjects. The combined effect increased almost linearly with increasing duration of exposure to the MT EMF. Thus, MT EMF exposure ~136 times below the official limit (ICNIRP 2020) exerts a genotoxic action even greater than that of a caffeine dose ~290 times above the corresponding limit. Therefore, with a reasonable approximation, the limit for MT EMFs should be lowered by at least 40000 times (136x290) for short-term exposures, and 4000000 times for long-term exposures.
The research of the influences of man-made electromagnetic fields on tick physiology has been very sparse and long neglected since the pioneer studies published in 1996 and 2000. Once multiple behavioral tests confirmed an attraction and possible perception of electromagnetic fields in ticks, a new interest in this topic erupted in recent years. In this study, qRT-PCR is utilized to determine the changes in the mRNA transcript levels of neuropeptides SIFamide and myoinhibitory peptide (mip and sifa) and their representative receptors (mip-r1 and sifa-r1) in the synganglia of the tick Ixodes ricinus irradiated by 900 MHz radiofrequency electromagnetic field. It was determined that 40 V/m intensity has a significant suppressory effect on the transcript levels of all genes after at least 60 minutes of constant exposure in both sexes. Commonly occurring intensity of radiation in urban areas (2 V/m) produced an elevation in mRNA levels after various timespans in every gene. A significant decrease of transcript abundances was detected in females after one hour of exposure to 2 V/m. Results of this study widen the knowledge of EMF-induced alterations in the neurophysiology of I. ricinus, the most commonly distributed hard tick in Europe.
Supplementary Information
The online version contains supplementary material available at 10.1007/s00436-024-08326-7.
This article provides a comprehensive analysis of the biological hazards associated with electromagnetic radiation (EMR) using mobile phones as a case study, aiming to dispel ambiguities and provide practical insights grounded in scientific evidence. Delving into the intricate interplay between EMR and living organisms, the authors explore various biological effects, including DNA damage, oxidative stress, and neurological impacts, substantiated by a wealth of research studies. The conflicting findings and controversies in EMR research are critically examined, shedding light on methodological differences, confounding variables, and ethical considerations. Regulatory guidelines, safety standards, and precautionary approaches are evaluated, emphasizing the need for international collaboration and continued research. Furthermore, the article clearly describes mitigation strategies at individual, community, and policy levels, empowering readers with practical measures to minimize EMR exposure while maximizing the benefits of modern technology.
This paper presents the mechanism of signal transformation by which a signal from the magnetic component of the low-frequency electromagnetic field with extremely low energy is changed into chemical and biochemical signals which elicit a biological response in aqueous solutions of biopolymers based on nucleic acids and proteins. A theoretical model developed shows that the basis of oxidative DNA damage and conformational transitions of proteins is a universal mechanism associated with a change in the amount of the most long-lived form - hydrogen peroxide in a chemical oscillator of mutual transformations of reactive oxygen species under the influence of low-intensity electromagnetic field exposure. It has been experimentally established that the quantitative content of hydrogen peroxide in solutions of biopolymers resonantly depends on the frequency of applied field. Conformational changes in proteins are accompanied by an increase in the availability and activity of the nucleophilic centers that are potential targets for reactive oxygen species. Complete unfolding and denaturation of the amino acid chain of the protein under the influence of low-frequency electromagnetic field exposure do not occur. It has been shown that enhanced hydrogen peroxide formation at 3 Hz and 50 Hz leads to oxidative modification of nitrogenous bases in DNA.
At the cellular level, stress can be defined as an array of processes that get sparked as a result of an external stimulus, thereby leading to acute or chronic deviation from the normal cellular milieu and homeostasis with the intent of negating the impairment together with fixing the injury, thereby ultimately safeguarding the cell or the organism against any insults. Therefore, the induction of stress response signifies the presence of the stressor and the induced damage; however, stress itself is not the insult. When exposed to a particular stress, the cells try to counter it in multiple ways, like the oxidative stress response system, heat shock response system, genotoxic response system, metabolic/energetic response system, hypoxia response system, and so on, which ensure the continuity or may lead to programmed cell death by way of which the injured cells are ultimately removed. So, the various cellular death mechanisms such as necrosis, apoptosis, etc., bank on the cell’s capacity to combat cellular stress.
Amaç: Bu çalışmanın amacı, kanda hematolojik ve biyokimyasal değişikliklere neden olabilen 2.45 GHz elektromanyetik radyasyonun (EMR) etkilerini araştırmaktır. EMR maruziyetinin etkilerine karşı koruyucu özelliği olan Vitamin C'yi (Vit C) tercih ettik. Materyal-Metot: Bu çalışma için 18 dişi Sprague Dawley sıçanı rastgele her birinde altı hayvan bulunan üç gruba ayrıldı: Kontrol, EMR ve EMR+Vit C grupları. Kontrol grubu: gavaj ile 30 gün boyunca 0.1 ml/gün salin; EMR grubu: EMR, 30 gün boyunca 1 saat/gün; EMR+Vit C grubu: EMR, 30 gün boyunca 1 saat/gün C vitamini 250 mg/kg/gün, gavaj ile. Beyaz Kan Hücresi (WBC), Nötrofil, Lenfosit, Monosit, Eozinofil, Bazofil, Kırmızı Kan Hücresi (RBC), Hemoglobin (Hb), Hematokrit (Htc), Ortalama Eritrosit Hacmi (MCV), Kırmızı Hücre Dağılım Genişliği-SD (RDW- SD), Kırmızı Hücre Dağılım Genişliği-CV (RDW-CV), Trombosit (PLT), Ortalama Trombosit Hacmi (MPV), Trombosit Dağılım Genişliği (PDW), Trombosit Krit (PCT) ve Trombosit Büyük Hücre Oranı (P-LCR) sayıları ölçülmüştür. Comet testi ile lenfosit DNA hasarı değerlendirildi, ayrıca malondialdehit (MDA) seviyesi ve katalaz (CAT) aktivitesi değerlendirildi. Bulgular: Comet analiz skoru ve P-LCR sayıları EMR grubunda Kontrol grubuna göre arttı (p<0,05). C vitamini tedavisi sonrası comet analiz skorunda ve P-LCR sayılarında EMR grubuna göre azalma gözlemledik (p<0,05). Sonuç: Sonuçlar, bir cep telefonu tarafından üretilen frekansta EMR'nin lenfosit DNA kırılmasına neden olduğunu ve P-LCR seviyesini artırdığını göstermektedir. C vitamini, EMF maruziyetinin neden olduğu lenfosit DNA hasarını ve P-LCR seviyesini azaltıyor gibi görünmektedir.
Increasing use of mobile phones in daily life with increasing adverse effects of electromagnetic radiation cause many concerns about their effects on human health. This study was designed to investigate the effect of exposure to a 900-MHz electromagnetic waves (EMW) produced by mobile phones on nucleic acids (DNA and RNA), protein content, kidney function (levels of urea and creatinine) and oxidative stress (malondialdehyde, MDA level) in rats before, during and after pregnancy periods and their offspring. A total of 32 Wistar albino female rats were divided into 4 equal groups (8 each): 1- unexposed (control group); 2- pre-pregnancy (2 h/d for 21 d) EMW-exposed group; 3- during pregnancy (2 h/d for 21 d) EMW-exposed group; 4- during and after pregnancy (2 h/d for each period) EMW-exposed group. Dams, new born and young rats (40-50 g) of all groups were sacrificed and kidney tissues were harvested for determination of parameters under investigation. A high significant decrease in DNA, RNA and protein levels were found of all periods in exposed groups compared to control. No difference in protein, DNA and RNA content in new born and young rats of pre-pregnancy EMW exposed rats, however these parameters were increased significantly in new born and young rats of both during and during and after pregnancy exposed groups compared to control. There was no difference in new born kidney function and oxidative stress of all exposed groups compared to control. However, these parameters were increased significantly in young rats of both during and during and after pregnancy exposed groups as well in all exposed groups compared to control. In conclusion, the EMW propagated from mobile phones have harmful effects on DNA, RNA and protein content as well kidney function and oxidative stress of exposed rats and their offspring. Therefore, people may use various antioxidants and avoid exposure to EMW for a long periods to prevent the potential adverse effects of exposure to EMW.
Much of the controversy over the cause of electrohypersensitivity (EHS) lies in the absence of recognized clinical and biological criteria for a widely accepted diagnosis. However, there are presently sufficient data for EHS to be acknowledged as a distinctly well-defined and objectively characterized neurologic pathological disorder. Because we have shown that 1) EHS is frequently associated with multiple chemical sensitivity (MCS) in EHS patients, and 2) that both individualized disorders share a common pathophysiological mechanism for symptom occurrence; it appears that EHS and MCS can be identified as a unique neurologic syndrome, regardless its causal origin. In this overview we distinguish the etiology of EHS itself from the environmental causes that trigger pathophysiological changes and clinical symptoms after EHS has occurred. Contrary to present scientifically unfounded claims, we indubitably refute the hypothesis of a nocebo effect to explain the genesis of EHS and its presentation. We as well refute the erroneous concept that EHS could be reduced to a vague and unproven “functional impairment”. To the contrary, we show here there are objective pathophysiological changes and health effects induced by electromagnetic field (EMF) exposure in EHS patients and most of all in healthy subjects, meaning that excessive non-thermal anthropogenic EMFs are strongly noxious for health. In this overview and medical assessment we focus on the effects of extremely low frequencies, wireless communications radiofrequencies and microwaves EMF. We discuss how to better define and characterize EHS. Taken into consideration the WHO proposed causality criteria, we show that EHS is in fact causally associated with increased exposure to man-made EMF, and in some cases to marketed environmental chemicals. We therefore appeal to all governments and international health institutions, particularly the WHO, to urgently consider the growing EHS-associated pandemic plague, and to acknowledge EHS as a new real EMF causally-related pathology.
Photodynamic therapy (PDT) offers several advantages for treating cancers, but its efficacy is highly dependent on light delivery to activate a photosensitizer. Advances in wireless technologies enable remote delivery of light to tumors, but suffer from key limitations, including low levels of tissue penetration and photosensitizer activation. Here, we introduce Dee-pLabCut (DLC)-informed low-power wireless telemetry with an integrated thermal/light simulation platform that overcomes the above constraints. The simulator produces an optimized combination of wavelengths and light sources, and DLC-assisted wireless telemetry uses the parameters from the simulator to enable adequate illumination of tumors through high-throughput (<20 mice) and multi-wavelength operation. Together, they establish a range of guidelines for effective PDT regimen design. In vivo Hypericin and Foscan mediated PDT, using cancer xenograft models, demonstrates substantial suppression of tumor growth, warranting further investigation in research and/or clinical settings.
2012-2018 - Peer Reviewed Published Research Studies On Wi-Fi And 2.4 GHz Wireless Frequencies
This article reviews the research progress of non-thermal disinfection technologies in food and introduces the principles of non-thermal disinfection technologies such as ultra-high pressure, ozone, acid electrolyzed water, irradiation, magnetic sterilization, high-pressure carbon dioxide, and natural antibacterial. We discuss the characteristics and application progress of non-thermal disinfection technologies in food processing and analyze their development trend based on their application and promotion in food processing and storage.
Exposure of animals/biological samples to human‑made electromagnetic fields (EMFs), especially in the extremely low frequency (ELF) band, and the microwave/radio frequency (RF) band which is always combined with ELF, may lead to DNA damage. DNA damage is connected with cell death, infertility and other pathologies, including cancer. ELF exposure from high‑voltage power lines and complex RF exposure from wireless communication antennas/devices are linked to increased cancer risk. Almost all human‑made RF EMFs include ELF components in the form of modulation, pulsing and random variability. Thus, in addition to polarization and coherence, the existence of ELFs is a common feature of almost all human‑made EMFs. The present study reviews the DNA damage and related effects induced by human‑made EMFs. The ion forced‑oscillation mechanism for irregular gating of voltage‑gated ion channels on cell membranes by polarized/coherent EMFs is extensively described. Dysfunction of ion channels disrupts intracellular ionic concentrations, which determine the cell's electrochemical balance and homeostasis. The present study shows how this can result in DNA damage through reactive oxygen species/free radical overproduction. Thus, a complete picture is provided of how human‑made EMF exposure may indeed lead to DNA damage and related pathologies, including cancer. Moreover, it is suggested that the non‑thermal biological effects attributed to RF EMFs are actually due to their ELF components.
Objective:
The global health crisis in the form of COVID-19 has forced people to shift their routine activities into a remote environment with the help of technology. The outbreak of the COVID-19 has caused several organizations to be shut down and forced them to initiate work from home employing technology. Now more than ever, it's important for people and institutions to understand the impact of excessive use of mobile phone technology and electronic gadgets on human health, cognition, and behavior. It is important to understand their perspective and how individuals are coping with this challenge in the wake of the COVID-19 pandemic. The investigation is an effort to answer the research question: whether dependency on technology during lockdown has more effects on human health in comparison to normal times.
Methods:
The study included participants from India (n = 122). A questionnaire was framed and the mode of conducting the survey chosen was online to maintain social distancing during the time of the Pandemic. The gathered data was statistically analysed employing RStudio and multiple regression techniques.
Results:
The statistical analysis confirms that lockdown scenarios have led to an increase in the usage of mobile phone technology which has been confirmed by around 90% of participants. Moreover, 95% of the participants perceive an increased risk of developing certain health problems due to excessive usage of mobile phones and technology. It has been evaluated that participants under the age group 15-30 years are highly affected (45.9%) during lockdown due to excessive dependence on technology. And, amongst different professions, participants involved in online teaching-learning are the most affected (42.6%).
Conclusion:
The findings indicate that dependency on technology during lockdown has more health effects as compared to normal times. So, it is suggested that as more waves of pandemics are being predicted, strategies should be planned to decrease the psychological and physiological effects of the overuse of technology during lockdown due to pandemics. As the lockdown situation unfolds, people and organization functioning styles should be rolled back to the limited dependency on technology.
Antibiotic-resistant bacteria (ARB) pose a substantial threat to public health worldwide. Electrochemistry, as a low energy consumption and environmentally friendly technique, is ideal for inactivating ARB. This study explored the utility of electrochemical disinfection (ED) for inactivating ARB (Escherichia coli K-12 LE392 resistant to kanamycin, tetracycline, and ampicillin) and the regrowth potential of the treated ARB. The results revealed that 5.12-log ARB removal was achieved within 30 min of applying molybdenum carbide as the anode and cathode material under a voltage of 2.0 V. No ARB regrowth was observed in the cathode chamber after 60 min of incubation in unselective broth, demonstrating that the process in the cathode chamber was more effective for permanent inactivation of ARB. The mechanisms underlying the ARB inactivation were verified based on intercellular reactive oxygen species (ROS) measurement, membrane integrity detection, and genetic damage assessment. Higher ROS production and membrane permeability were observed in the cathode and anode groups (p < 0.001) compared to the control group (0 V). In addition, the DNA was more likely to be damaged during the ED process. Collectively, our results demonstrate that ED is a promising technology for disinfecting water to prevent the spread of ARB.
Over the last decade, the exponential growth of mobile communication has been accompanied by a parallel increase in density of electromagnetic fields (EMF). The continued expansion of mobile phone usage raises important questions as EMF, especially radio frequency (RF), have long been suspected of having biological effects. Because mobile phones and other wireless gadgets are held close to the body and are also used very frequently, these devices are potentially the most dangerous sources of EM radiation. This gave rise to an increasing concern for any unknown effects that may prove to be detrimental to human health.
In addition to excessive use of chemical and physical antiseptics in food, any harmful microorganisms present in food are potentially the cause of food safety issues and even cause foodborne diseases to threaten human health. Thermal processing of food as a conventional sterilization technology has been widely used in the food industry to ensure food safety. However, heat treatment has some inevitable adverse effects on nutrition, flavor, color, texture, and aesthetics of the food products. Therefore, it is necessary to research novel nonthermal, green technologies to minimize the impact of undesirable changes on food, and enhance the inactivation efficiency of microorganisms that can cause foodborne illnesses. This review presents a general perspective of the pulsed magnetic field (PMF) as a novel nonthermal sterilization technology. The operating principle, characteristics, and biological effects on microorganisms of PMF are described. Furthermore, the possible inactivation mechanisms and their application in food processing are also addressed. PMF sterilization is considered to be an effective and efficient microorganism eliminating technology that exerts its germicidal ability by magnetoporation and electromagnetic effects, mainly including induced current effect, Lorentz force effect, oscillation effect, and ionization effect. Compared to thermal treatment, PMF sterilization technique meets the requirements of commercial food sterilization standards without impacting food flavor, taste, and texture. The findings of our review suggest that PMF itself would be beneficial as a bacteria inactivation technique or could be readily combined with other suitable methods. Besides, we recommend conceivable paths to adopt this sustainable technique in the food industry.
Objective:
To evaluate the effect of contrast enhanced abdominopelvic magnetic resonance imaging (MRI), using a 3 Tesla scanner, on expression and methylation level of ATM and AKT genes in human peripheral blood lymphocytes.
Materials and methods:
In this prospective in vivo study, blood samples were obtained from 20 volunteer patients with mean age of 43 ± 8 years (range 32-68 years) before contrast enhanced MRI, 2 hours and 24 hours after contrast enhanced abdominopelvic 3 Tesla MRI. After separation of mononuclear cells from peripheral blood, using Ficoll-Hypaque, we analyzed gene expression changes of ATM and AKT genes 2 hours and 24 hours after MRI using quantitative reverse transcription polymerase chain reaction (qRT-PCR). We also evaluated methylation percentage of the above mentioned genes in before, 2 hours and 24 hours after MRI, using MethySYBR method.
Results:
Fold change analysis, in comparison with the baseline, respectively showed 1.1 ± 0.7 and 0.8 ± 0.5 mean of gene expressions in 2 and 24 hours after MRI for ATM, while the results were 1.4 ± 0.6 and 1.4 ± 1 for AKT (P>0.05). Methylation of the ATM gene promoter were 8.8 ± 1.5%, 9 ± 0.6% and 9 ± 0.8% in before contrast enhanced MRI, 2 and 24 hours after contrast enhanced MRI, respectively (P>0.05). Methylation of AKT gene promoter in before contrast enhanced MRI, 2 hours and 24 hours after contrast enhanced MRI was 5.4 ± 2.5, 5 ± 3.2, 4.9 ± 2.9 respectively (P>0.05).
Conclusion:
Contrast enhanced abdominopelvic MRI using 3 Tesla scanner apparently has no negative effect on the expression and promoter methylation level of ATM and AKT genes involved in the repair pathways of genome.
Ambient levels of nonionizing electromagnetic fields (EMF) have risen sharply in the last five decades to become a ubiquitous, continuous, biologically active environmental pollutant, even in rural and remote areas. Many species of flora and fauna, because of unique physiologies and habitats, are sensitive to exogenous EMF in ways that surpass human reactivity. This can lead to complex endogenous reactions that are highly variable, largely unseen, and a possible contributing factor in species extinctions, sometimes localized. Non-human magnetoreception mechanisms are explored. Numerous studies across all frequencies and taxa indicate that current low-level anthropogenic EMF can have myriad adverse and synergistic effects, including on orientation and migration, food finding, reproduction, mating, nest and den building, territorial maintenance and defense, and on vitality, longevity and survivorship itself. Effects have been observed in mammals such as bats, cervids, cetaceans, and pinnipeds among others, and on birds, insects, amphibians, reptiles, microbes and many species of flora. Cyto- and geno-toxic effects have long been observed in laboratory research on animal models that can be extrapolated to wildlife. Unusual multi-system mechanisms can come into play with non-human species — including in aquatic environments — that rely on the Earth’s natural geomagnetic fields for critical life-sustaining information. Part 2 of this 3-part series includes four online supplement tables of effects seen in animals from both ELF and RFR at vanishingly low intensities. Taken as a whole, this indicates enough information to raise concerns about ambient exposures to nonionizing radiation at ecosystem levels. Wildlife loss is often unseen and undocumented until tipping points are reached. It is time to recognize ambient EMF as a novel form of pollution and develop rules at regulatory agencies that designate air as ‘habitat’ so EMF can be regulated like other pollutants. Long-term chronic low-level EMF exposure standards, which do not now exist, should be set accordingly for wildlife, and environmental laws should be strictly enforced — a subject explored in Part 3.
Intense electromagnetic fields (EMFs) induce DNA double stranded breaks (DSBs) in exposed lymphocytes.We study developing pre-B lymphocytes following V(D)J recombination at their Immunoglobulin light chain loci (IgL). Recombination physiologically induces DNA DSBs, and we tested if low doses of EMF irradiation affect this developmental stage. Recombining pre-B cells, were exposed for 48 h to low intensity EMFs (maximal radiative power density flux S of 9.5 µW/cm2 and electric field intensity 3 V/m) from waves of frequencies ranging from 720 to 1224 MHz. Irradiated pre-B cells show decreased levels of recombination, reduction which is dependent upon the power dose and most remarkably upon the frequency of the applied EMF. Although 50% recombination reduction cannot be obtained even for an S of 9.5 µW/cm2 in cells irradiated at 720 MHz, such an effect is reached in cells exposed to only 0.45 µW/cm2 power with 950 and 1000 MHz waves. A maximal four-fold recombination reduction was measured in cells exposed to 1000 MHz waves with S from 0.2 to 4.5 µW/cm2 displaying normal levels of γH2AX phosphorylated histone. Our findings show that developing B cells exposure to low intensity EMFs can affect the levels of production and diversity of their antibodies repertoire.
Electromagnetic radiation from communication and electronic devices, networks, systems and base stations has drawn concern due to excessive global usage with increasing power and operating frequency level. Numerous previous researches only focus on how the radiation from certain frequency ranges of particular devices could harm specific human organs and tissues, resulting in distinct symptoms. In this research, electromagnetic propagation and properties in 14 human organs and tissues were analyzed and investigated based on the organs and tissues' electromagnetic and mechanical parameters, and chemical composition. Counting the organs and tissues as electromagnetic materials, their permittivity and conductivity, computed by a 4-Cole-Cole mode, directly respective to the operating frequency, are interrelated to wave behavior and hence influence the organs' response. Tests were conducted in 1 GHz to 105 GHz system settings, covering most microwave frequency uses: 2.4 GHz of 4G-LTE, Wi-Fi, Bluetooth, ZigBee and the 5G ranges: 28 GHz of 5G-mmW and 95 GHz of 5G-IoT. Trial human organs and tissues were placed in the wave propagation direction of 2.4 GHz and 28 GHz dipole antennas, and a waveguide port operating from 95 to 105 GHz. The quantitative data on the effects of 5G penetration and dissipation within human tissues are presented. The absorbance in all organs and tissues is significantly higher as frequency increases. As the wave enters the organ-tissue model, the wavelength is shortened due to the high organ-tissue permittivity. Skin-Bone-Brain layer simulation results demonstrate that both electric and magnetic fields vanish before passing the brain layer at all three focal frequencies of 2.4 GHz, 28 GHz and 100 GHz.
The debate on the biological effects of radiofrequency radiation (RFR) still continues due to differences in the design of studies (frequency, power density, specific absorption rate [SAR], exposure duration, cell, tissue, or animal type). The current study aimed to investigate the effects of 2,600 MHz RFR and melatonin on brain tissue biochemistry and histology of male rats. Thirty‐six rats were divided into six groups randomly: cage‐control, sham, RFR, melatonin, sham melatonin, and RFR melatonin. In RFR groups, animals were exposed to 2,600 MHz RFR for 30 days (30 min/day, 5 days/week) and the melatonin group animals were subcutaneously injected with melatonin (7 days/week, 10 mg/kg/day) for 30 days. SAR in brain gray matter was calculated as 0.44 and 0.295 W/kg for 1 and 10 g averaging, respectively. RFR exposure decreased the GSH, GSH‐Px, and SOD levels and increased the MPO, MDA, and NOx levels (P < 0.005) significantly. RFR exposure also led to an increase in structural deformation and apoptosis in the brain tissue. This study revealed that exogenous high‐dose melatonin could reduce these adverse effects of RFR. Limiting RFR exposure as much as possible is recommended, and taking daily melatonin supplements may be beneficial. Bioelectromagnetics. © 2021 Bioelectromagnetics Society
The continuously increasing usage of cell phones has raised concerns about the adverse effects of microwave radiation (MWR) emitted by cell phones on health. Several in vitro and in vivo studies have claimed that MWR may cause various kinds of damage in tissues. The aim of this study is to examine the possible effects of exposure to low‐intensity MWR on DNA and oxidative damage in the livers of rats. Eighteen Sprague–Dawley male rats were divided into three equal groups randomly (n = 6). Group 1 (Sham‐control): rats were kept under conditions the same as those of other groups, except for MWR exposure. Group 2: rats exposed to 1800 MHz (SAR: 0.62 W/kg) at 0.127 ± 0.04 mW/cm2 power density, and Group 3: rats exposed to 2,100 MHz (SAR: 0.2 W/kg) at 0.038 ± 0.03 mW/cm2 power density. Microwave application groups were exposed to MWR 2 h/day for 7 months. At the end of the exposure period, the rats were sacrificed and DNA damage, malondialdehyde (MDA), 8‐hydroxydeoxyguanosine (8‐OHdG), and total oxidant‐antioxidant parameter analyses were conducted in their liver tissue samples. It was found that 1800 and 2100 MHz low‐intensity MWR caused a significant increase in MDA, 8‐OHdG, total oxidant status, oxidative stress index, and comet assay tail intensity (P < 0.05), while total antioxidant status levels (P < 0.05) decreased. The results of our study showed that whole‐body exposure to 1800 and 2100 MHz low‐intensity MWR emitted by cell phones can induce oxidative stress by altering oxidant‐antioxidant parameters and lead to DNA strand breaks and oxidative DNA damage in the liver of rats. Bioelectromagnetics. © 2020 Bioelectromagnetics Society
Keywords: microwave radiation; liver; DNA damage; 8‐OHdG; MDA
The role of protein kinase C PKC in B cell activation is controversial. These studies were undertaken to determine whether protein kinase C has a stimulatory or inhibitory role in B cell activation. We found that treatment of B cells for a short period of time (30 min) with the PKC activator phorbol 12,13-dibutyrate (PDBU) primed the cells for enhanced proliferative responses to anti-immunoglobulin (anti-Ig) antibody whereas treatment for a longer period of time (3 h or more) resulted in suppression of proliferation. The enhanced proliferative response to treatment of B cells with PDBU for short periods of time was associated with inhibition of anti-Ig-stimulated increases in phosphatidyl 4,5-bisphosphate (PIP2) hydrolysis and inhibition of increases in [Ca²⁺]i, indicating that activation of PKC per se might be sufficient for enhancing B cell activation. The time-dependent effect of phorbol esters on the inhibition of B cell proliferation was found to be closely correlated with the kinetics of disappearance of PKC as measured by Western blot and by enzymatic activity but not with inhibition of [Ca²⁺]i and PIP2. These data demonstrate a bimodal time-dependent effect of PDBU on B cell activation and suggest that (a) the inhibitory effect of phorbol ester on anti-Ig-induced proliferation may be due to the disappearance of PKC rather than to the inhibition of PIP2 and Ca²⁺; and (b) the early activation of PKC is a stimulatory rather than an inhibitory signal in the induction of B lymphocyte proliferation by anti-Ig.
There is public concern that use of mobile phones could increase the risk of brain tumours. If such an effect exists, acoustic neuroma would be of particular concern because of the proximity of the acoustic nerve to the handset. We conducted, to a shared protocol, six population-based case–control studies in four Nordic countries and the UK to assess the risk of acoustic neuroma in relation to mobile phone use. Data were collected by personal interview from 678 cases of acoustic neuroma and 3553 controls. The risk of acoustic neuroma in relation to regular mobile phone use in the pooled data set was not raised (odds ratio (OR)=0.9, 95% confidence interval (CI): 0.7–1.1). There was no association of risk with duration of use, lifetime cumulative hours of use or number of calls, for phone use overall or for analogue or digital phones separately. Risk of a tumour on the same side of the head as reported phone use was raised for use for 10 years or longer (OR=1.8, 95% CI: 1.1–3.1). The study suggests that there is no substantial risk of acoustic neuroma in the first decade after starting mobile phone use. However, an increase in risk after longer term use or after a longer lag period could not be ruled out.Keywords: neuroma, acoustic, telephone, epidemiology, aetiology
The data on biologic effects of nonthermal microwaves (MWs) from mobile telephones are diverse, and these effects are presently ignored by safety standards of the International Commission for Non-Ionizing Radiation Protection (ICNIRP). In the present study, we investigated effects of MWs of Global System for Mobile Communication (GSM) at different carrier frequencies on human lymphocytes from healthy persons and from persons reporting hypersensitivity to electromagnetic fields (EMFs). We measured the changes in chromatin conformation, which are indicative of stress response and genotoxic effects, by the method of anomalous viscosity time dependence, and we analyzed tumor suppressor p53-binding protein 1 (53BP1) and phosphorylated histone H2AX (gamma-H2AX), which have been shown to colocalize in distinct foci with DNA double-strand breaks (DSBs), using immunofluorescence confocal laser microscopy. We found that MWs from GSM mobile telephones affect chromatin conformation and 53BP1/gamma-H2AX foci similar to heat shock. For the first time, we report here that effects of MWs from mobile telephones on human lymphocytes are dependent on carrier frequency. On average, the same response was observed in lymphocytes from hypersensitive and healthy subjects.
BACKGROUND: The impact of microwave (MW)/radio frequency radiation (RFR) on important biological parameters is probably more than a simply thermal one. Exposure to radio frequency (RF) signals generated by the use of cellular telephones have increased dramatically and reported to affect physiological, neurological, cognitive and behavioural changes and to induce, initiate and promote carcinogenesis. Genotoxicity of RFR has also been reported in various test systems after in vitro and/or in vivo exposure but none in mobile phone users. AIMS: In the present study, DNA and chromosomal damage investigations were carried out on the peripheral blood lymphocytes of individuals using mobile phones, being exposed to MW frequency ranging from 800 to 2000 MHz. METHODS: DNA damage was assessed using the single cell gel electrophoresis assay and aneugenic and clastogenic damage by the in vivo capillary blood micronucleus test (MNT) in a total of 24 mobile phone users. RESULTS: Mean comet tail length (26.76 ± 0.054 mm; 39.75% of cells damaged) in mobile phone users was highly significant from that in the control group. The in vivo capillary blood MNT also revealed highly significant (0.25) frequency of micronucleated (MNd) cells. CONCLUSIONS: These results highlight a correlation between mobile phone use (exposure to RFR) and genetic damage and require interim public health actions in the wake of widespread use of mobile telephony.
BACKGROUND: The impact of microwave (MW)/radio frequency radiation (RFR) on important biological parameters is probably more than a simply thermal one. Exposure to radio frequency (RF) signals generated by the use of cellular telephones have increased dramatically and reported to affect physiological, neurological, cognitive and behavioural changes and to induce, initiate and promote carcinogenesis. Genotoxicity of RFR has also been reported in various test systems after in vitro and/or in vivo exposure but none in mobile phone users. AIMS: In the present study, DNA and chromosomal damage investigations were carried out on the peripheral blood lymphocytes of individuals using mobile phones, being exposed to MW frequency ranging from 800 to 2000 MHz. METHODS: DNA damage was assessed using the single cell gel electrophoresis assay and aneugenic and clastogenic damage by the in vivo capillary blood micronucleus test (MNT) in a total of 24 mobile phone users. RESULTS: Mean comet tail length (26.76 ± 0.054 mm; 39.75% of cells damaged) in mobile phone users was highly significant from that in the control group. The in vivo capillary blood MNT also revealed highly significant (0.25) frequency of micronucleated (MNd) cells. CONCLUSIONS: These results highlight a correlation between mobile phone use (exposure to RFR) and genetic damage and require interim public health actions in the wake of widespread use of mobile telephony.
The role of protein kinase C PKC in B cell activation is controversial. These studies were undertaken to determine whether protein kinase C has a stimulatory or inhibitory role in B cell activation. We found that treatment of B cells for a short period of time (30 min) with the PKC activator phorbol 12,13-dibutyrate (PDBU) primed the cells for enhanced proliferative responses to anti-immunoglobulin (anti-Ig) antibody whereas treatment for a longer period of time (3 h or more) resulted in suppression of proliferation. The enhanced proliferative response to treatment of B cells with PDBU for short periods of time was associated with inhibition of anti-Ig-stimulated increases in phosphatidyl 4,5-bisphosphate (PIP2) hydrolysis and inhibition of increases in [Ca2+]i, indicating that activation of PKC per se might be sufficient for enhancing B cell activation. The time-dependent effect of phorbol esters on the inhibition of B cell proliferation was found to be closely correlated with the kinetics of disappearance of PKC as measured by Western blot and by enzymatic activity but not with inhibition of [Ca2+]i and PIP2. These data demonstrate a bimodal time-dependent effect of PDBU on B cell activation and suggest that (a) the inhibitory effect of phorbol ester on anti-Ig-induced proliferation may be due to the disappearance of PKC rather than to the inhibition of PIP2 and Ca2+; and (b) the early activation of PKC is a stimulatory rather than an inhibitory signal in the induction of B lymphocyte proliferation by anti-Ig.
The effects of topoisomerase II-reactive epipodophyllotoxins etoposide and teniposide as well as amsacrine on the viability of thymocytes in primary culture has been examined. All three drugs were shown to produce DNA cleavage detectable by resolving isolated DNA by pulsed field agarose gel electrophoresis. The DNA cleavage was found to have two components. The first was due to the interaction of the drugs with topoisomerase II, whereas the second component was due to endonuclease cleavage caused by the drug-induced entry of the thymocytes into programmed cell death or apoptosis. This second component of the DNA cleavage was also detected in thymocytes undergoing apoptosis following exposure to the glucocorticoid analogue, dexamethasone. The effect of the drugs on programmed cell death is dependent upon new protein and RNA synthesis, indicating that topoisomerase II has a role in the very first stages of the process. These results are discussed in terms of the use of this class of topoisomerase II-reactive drugs in chemotherapy.
Levels of DNA single-strand break were assayed in brain cells from rats acutely exposed to low-intensity 2450 MHz microwaves using an alkaline microgel electrophoresis method. Immediately after 2 h of exposure to pulsed (2 microseconds width, 500 pulses/s) microwaves, no significant effect was observed, whereas a dose rate-dependent [0.6 and 1.2 W/kg whole body specific absorption rate (SAR)] increase in DNA single-strand breaks was found in brain cells of rats at 4 h postexposure. Furthermore, in rats exposed for 2 h to continuous-wave 2450 MHz microwaves (SAR 1.2 W/kg), increases in brain cell DNA single-strand breaks were observed immediately as well as at 4 h postexposure.
We investigated the effects of acute (2-h) exposure to pulsed (2-micros pulse width, 500 pulses s(-1)) and continuous wave 2450-MHz radiofrequency electromagnetic radiation on DNA strand breaks in brain cells of rat. The spatial averaged power density of the radiation was 2mW/cm2, which produced a whole-body average-specific absorption rate of 1.2W/kg. Single- and double-strand DNA breaks in individual brain cells were measured at 4h post-exposure using a microgel electrophoresis assay. An increase in both types of DNA strand breaks was observed after exposure to either the pulsed or continuous-wave radiation, No significant difference was observed between the effects of the two forms of radiation. We speculate that these effects could result from a direct effect of radiofrequency electromagnetic energy on DNA molecules and/or impairment of DNA-damage repair mechanisms in brain cells. Our data further support the results of earlier in vitro and in vivo studies showing effects of radiofrequency electromagnetic radiation on DNA.
Recent reports suggest that exposure to 2450 MHz electromagnetic radiation causes DNA single-strand breaks (SSBs) and double-strand breaks (DSBs) in cells of rat brain irradiated in vivo (Lai and Singh, Bioelectromagnetics 16, 207-210, 1995; Int. J. Radiat. Biol. 69, 513-521, 1996). Therefore, we endeavored to determine if exposure of cultured mammalian cells in vitro to 2450 MHz radiation causes DNA damage. The alkaline comet assay (single-cell gel electrophoresis), which is reportedly the most sensitive method to assay DNA damage in individual cells, was used to measure DNA damage after in vitro 2450 MHz irradiation. Exponentially growing U87MG and C3H 10T1/2 cells were exposed to 2450 MHz continuous-wave (CW) radiation in specially designed radial transmission lines (RTLs) that provided relatively uniform microwave exposure. Specific absorption rates (SARs) were calculated to be 0.7 and 1.9 W/kg. Temperatures in the RTLs were measured in real time and were maintained at 37 +/- 0.3 degrees C. Every experiment included sham exposure(s) in an RTL. Cells were irradiated for 2 h, 2 h followed by a 4-h incubation at 37 degrees C in an incubator, 4 h and 24 h. After these treatments samples were subjected to the alkaline comet assay as described by Olive et al. (Exp. Cell Res. 198, 259-267, 1992). Images of comets were digitized and analyzed using a PC-based image analysis system, and the "normalized comet moment" and "comet length" were determined. No significant differences were observed between the test group and the controls after exposure to 2450 MHz CW irradiation. Thus 2450 MHz irradiation does not appear to cause DNA damage in cultured mammalian cells under these exposure conditions as measured by this assay.
The DNA repair protein O6-methylguanine-DNA methyltransferase (MGMT) is inducible by genotoxic stress. MGMT induction results from transcriptional activation of the MGMT gene which is a specific response to DNA damage. A possible factor involved in triggering MGMT induction might be p53, because both p53 and MGMT are activated by DNA breaks. To study the effect of p53 on induction of the MGMT gene, we compared the presence of functional wild-type (wt) and mutant p53 with MGMT expression level in various mouse fibroblasts and rat hepatoma cell lines upon genotoxic treatment. Cells which responded to ionizing radiation (IR) by MGMT induction displayed functional p53, whereas in cells not expressing wt p53, MGMT induction was not observed. Also, the cloned MGMT promoter was inducible by IR upon transfection into p53 wt cells, but not in cells deficient for p53. Thus, expression of wt p53 appears to be required for induction of MGMT mRNA and protein by IR. On the other hand, transfection of a MGMT-promoter-CAT construct together with p53 (either wt or mutant) in cells expressing wt p53 markedly reduced the basal activity of the MGMT promoter whereas cotransfection with a p53 antisense construct slightly increased MGMT promoter activity. Furthermore, cotransfection of MGMT promoter with wt or mutant p53 in p53 wt cells reduced radiation evoked MGMT promoter induction. Thus, transfection mediated high level expression of p53 has inhibitory effect both on basal MGMT promoter activity and its activation by IR. The results give evidence for involvement of p53 in DNA damage-induced MGMT promoter activation.
The present study describes modifications to the basic comet protocol that increase productivity and efficiency without sacrificing assay reliability. A simple technique is described for rapidly preparing up to 96 comet assay samples simultaneously. The sample preparation technique allows thin layers of agarose-embedded cells to be prepared in multiple wells attached to a flexible film of Gelbond, which improves the ease of manipulating and processing samples. To evaluate the effect of these modifications on assay sensitivity, dose-response curves are presented for DNA damage induced by exposure of TK6 cells to low concentrations of hydrogen peroxide (0-10 microM) and for exposure of human lymphocytes to X-irradiation (0-100 cGy). The limit of detection of DNA damage induced by hydrogen peroxide in TK6 cells was observed to be 1 uM for all parameters (tail ratio, tail moment, tail length and comet length) while the limit of detection of DNA damage in human lymphocytes was 10 cGy for tail and comet length parameters, but 50 cGy for tail ratio and tail moment parameters. These results are similar to those previously reported using the conventional alkaline comet assay. The application of SYBR Gold for detection of DNA damage was compared to that of propidium iodide. Measurements of matching samples for tail length and comet length were similar using both stains. However, comets stained with SYBR Gold persisted longer and were much brighter than those obtained with propidium iodide. SYBR Gold was found to be ideal for measuring tail length and comet length but, under present assay conditions, impractical for measuring tail ratio or tail moment due to saturation of staining in the head region of the comets.
The kappa -opioid agonists U50488H, bremazocine, and BRL52537, and the mu -opioid agonist morphine were compared in their ability to modify spontaneous motor activity in male NMRI mice. Higher, analgesic doses of the kappa -agonists reduced rearing, motility, and locomotion in nonhabituated mice. These effects, as well as the analgesic action of U50488H, were blocked by the selective kappa -opioid antagonists nor-binaltorphimine and DIPPA. In contrast, lower, subanalgesic doses (1.25 and 2.5 mg/kg for U50488H; 0.15 and 0.075 mg/kg for bremazocine, and 0.1 mg/kg for BRL52537) time dependently increased motor activity. The stimulatory effects of U50488H and bremazocine were not observed in habituated animals and were reduced by dopamine depletion. Surprisingly, the stimulatory effects of U50488H and bremazocine were not blocked by nor-binaltorphimine and DIPPA but they were completely eliminated by naloxone (0.1 mg/kg). The effects of morphine were dose-dependent; an initial limited suppression was followed by increased motility and locomotion (but not rearing) with a peak effect at 20 mg/kg both in habituated and nonhabituated mice. The selective mu -opioid antagonist beta -funaltrexamine blocked morphine-induced motor stimulation and analgesia but failed to affect the analgesic and motor stimulatory effects of U50488H. The results indicate that kappa -opioid agonists interact with different functional subtypes of opioid receptors. A stimulatory, naloxone-sensitive but nor-binaltorphimine- and DIPPA-insensitive subtype of opioid receptor appears to operate only when the dopamine system is tonically active in nonhabituated animals. At higher doses, kappa -agonists produce analgesia and motor suppression, effects mediated by a "classic" (inhibitory) kappa -opioid receptor.
There is convincing evidence that cellular prooxidant states--that is, increased concentrations of active oxygen and organic peroxides and radicals--can promote initiated cells to neoplastic growth. Prooxidant states can be caused by different classes of agents, including hyperbaric oxygen, radiation, xenobiotic metabolites and Fenton-type reagents, modulators of the cytochrome P-450 electron-transport chain, peroxisome proliferators, inhibitors of the antioxidant defense, and membrane-active agents. Many of these agents are promoters or complete carcinogens. They cause chromosomal damage by indirect action, but the role of this damage in carcinogenesis remains unclear. Prooxidant states can be prevented or suppressed by the enzymes of the cellular antioxidant defense and low molecular weight scavenger molecules, and many antioxidants are antipromoters and anticarcinogens. Finally, prooxidant states may modulate the expression of a family of prooxidant genes, which are related to cell growth and differentiation, by inducing alterations in DNA structure or by epigenetic mechanisms, for example, by polyadenosine diphosphate-ribosylation of chromosomal proteins.
The aging process is best defined as a general loss in biological competence for both the individual cell and the organism as a whole. At the cellular level, this loss is expressed as decreasing replicative ability in proliferating cells and decreasing functional activity in postmitotic cells (Little, 1976). For the organism, the aging process expresses itself as decreased viability and increased vulnerability to the normal forces of mortality (Goldstein, 1971a).
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Summary The activity of 0.01-1 µM of melatonin on depolarization-induced45Ca2+ influx by hypothalamic synaptosomes of rats killed at late evening (2000 h) depended on melatonin preincubation time, exhibiting an early (10 min) stimulation of uptake and an inhibition after 30 min of incubation. Both stimulatory and inhibitory effects were maximal at 2000 h and tended to a minimum at 2400 h, exhibiting intermediate values at 400 h. At 1000 h, only inhibitory effects of melatonin (1 µM) on Ca2+ uptake were found
Many reports in the literature have suggested the effect of exposure to radiofrequency electromagnetic radiation (RFR) (10 kHz-300,000 MHz) on the functions of the nervous system. Such effects are of great concern to researchers in bioelectromagnetics, since the nervous system coordinates and controls an organism’s responses to the environment through autonomic and voluntary muscular movements and neurohumoral functions. As it was suggested in the early stages of bioelectromagnetics research, behavioral changes could be the most sensitive effects of RFR exposure. At the summary of session B of the proceedings of an international symposium held in Warsaw, Poland, in 1973, it was stated that “The reaction of the central nervous system to microwaves may serve as an early indicator of disturbances in regulatory functions of many systems” [Czerski et al., 1974].
The effect of a temporally incoherent magnetic field noise on microwave-induced DNA single and double strand breaks in rat brain cells was investigated. Four treatment groups of rats were studied: microwave-exposure (continuous-wave 2450-MHz microwaves, power density 1 mW/cm2, average whole-body specific absorption rate of 0.6 W/kg), noise-exposure (45 mG), microwave + noise-exposure, and sham-exposure. Animals were exposed to these conditions for 2h. DNA single- and double-strand breaks in brain cells of these animals were assayed 4h later using a microgel electrophoresis assay. Results show that brain cells of microwave-exposed rats had significantly higher levels of DNA single- and double-strand breaks when compared with sham-exposed animals. Exposure to noise alone did not significantly affect the levels (i.e., they were similar to those of the sham-exposed rats). However, simultaneous noise exposure blocked microwave-induced increases in DNA strand breaks. These data indicate that simultaneous exposure to a temporally incoherent magnetic field could block microwave-induced DNA damage in brain cells of the rat.
This study has determined the sensitivity of the alkaline comet assay for the detection of strand breaks in the DNA of cells taken from a whole organism rather than a single cell type as in previously reported studies. The assay has been performed on cells from whole zebrafish larvae irradiated for 1 or 24 h at dose rates of 0.4, 1.2 or 7.2 mGy/h. Zebrafish larvae exposed to only 1.2 mGy/h of gamma-radiation for 1h showed a statistically significant increase in DNA damage compared to controls. This represents a high sensitivity of this animal model for DNA damage and of the comet assay protocol used for detecting such damage. Increasing the exposure time from 1 to 24 h caused significant increases in DNA damage in zebrafish larvae, although the modest size of these increases in damage for the relatively large increases (24 times) in total absorbed dose indicates that dose rate may be the major factor in determining the level of DNA damage observed under the conditions of these experiments.
The present study was undertaken to verify a hypothesis that exposure of the cells to static or 50 Hz magnetic fields (MF) and simultaneous treatment with a known oxidant, ferrous chloride, may affect the oxidative deterioration of DNA molecules.The comet assay was chosen for the assessment of DNA damage. The experiments were performed on isolated rat lymphocytes incubated for 3 h in Helmholtz coils at 7 mT static or 50 Hz MF. During MF exposure, part of the cell samples were incubated with 0.01 μM H2O2 and another one with 10 μg/ml FeCl2, the rest serving as controls.Lymphocyte exposure to MF at 7 mT did not increase the number of cells with DNA damage in the comet assay. Incubation of lymphocytes with 10 μg/ml FeCl2 did not produce a detectable damage of DNA either. However, when the FeCl2-incubated lymphocytes were simultaneously exposed to 7 mT MF, the number of damaged cells was significantly increased and reached about 20% for static MF and 15% for power frequency MF. In the control samples about 97% of the cells did not have any DNA damage.It is not possible at present to offer a reasonable explanation for the findings of this investigation — the high increase in the number of lymphocytes showing symptoms of DNA damage in the comet assay, following simultaneous exposure to the combination of two non-cytotoxic factors —10 μg/ml FeCl2 and 7 mT MF. In view of the obtained results we can only hypothesise that under the influence of simultaneous exposure to FeCl2 and static or 50 Hz MF, the number of reactive oxygen species generated by iron cations may increase substantially. Further studies will be necessary to confirm this hypothesis and define the biological significance of the observed effect.
We have previously shown that simultaneous exposure of rat lymphocytes to iron ions and 50 Hz magnetic field (MF) caused an increase in the number of cells with DNA strand breaks. Although the mechanism of MF-induced DNA damage is not known, we suppose that it involves free radicals. In the present study, to confirm our hypothesis, we have examined the effect of melatonin, an established free radicals scavenger, on DNA damage in rat peripheral blood lymphocytes exposed in vitro to iron ions and 50 Hz MF.The alkaline comet assay was chosen for the assessment of DNA damage. During pre-incubation, part of the cell samples were supplemented with melatonin (0.5 or 1.0 mM). The experiments were performed on the cell samples incubated for 3 h in Helmholtz coils at 7 mT 50 Hz MF. During MF exposure, some samples were treated with ferrous chloride (FeCl2, 10 μg/ml), while the rest served as controls.A significant increase in the number of cells with DNA damage was found only after simultaneous exposure of lymphocytes to FeCl2 and 7 mT 50 Hz MF, compared to the control samples or those incubated with FeCl2 alone. However, when the cells were treated with melatonin and then exposed to iron ions and 50 Hz MF, the number of damaged cells was significantly reduced, and the effect depended on the concentration of melatonin. The reduction reached about 50% at 0.5 mM and about 100% at 1.0 mM. Our results indicate that melatonin provides protection against DNA damage in rat lymphocytes exposed in vitro to iron ions and 50 Hz MF (7 mT). Therefore, it can be suggested that free radicals may be involved in 50 Hz magnetic field and iron ions-induced DNA damage in rat blood lymphocytes.The future experimental studies, in vitro and in vivo, should provide an answer to the question concerning the role of melatonin in the free radical processes in the power frequency magnetic field.
Molt-4 T-lymphoblastoid cells have been exposed to pulsed signals at cellular telephone frequencies of 813.5625 MHz (iDEN® signal) and 836.55 MHz (TDMA signal). These studies were performed at low SAR (average=2.4 and 24 μW g−1 for iDEN® and 2.6 and 26 μW g−1 for TDMA) in studies designed to look for athermal RF effects. The alkaline comet, or single cell gel electrophoresis, assay was employed to measure DNA single-strand breaks in cell cultures exposed to the radiofrequency (RF) signal as compared to concurrent sham-exposed cultures. Tail moment and comet extent were calculated as indicators of DNA damage. Statistical differences in the distribution of values for tail moment and comet extent between exposed and control cell cultures were evaluated with the Kolmogorov–Smirnoff distribution test. Data points for all experiments of each exposure condition were pooled and analyzed as single groups. It was found that: 1) exposure of cells to the iDEN® signal at an SAR of 2.4 μW g−1 for 2 h or 21 h significantly decreased DNA damage; 2) exposure of cells to the TDMA signal at an SAR of 2.6 μW g−1 for 2 h and 21 h significantly decreased DNA damage; 3) exposure of cells to the iDEN® signal at an SAR of 24 μW g−1 for 2 h and 21 h significantly increased DNA damage; 4) exposure of cells to the TDMA signal at an SAR of 26 μW g−1 for 2 h significantly decreased DNA damage. The data indicate a need to study the effects of exposure to RF signals on direct DNA damage and on the rate at which DNA damage is repaired.
Microwaves are shown to affect the kinetics of conformational changes of the protein beta-lactoglobulin. Microwaves can accelerate conformational changes in the direction towards the equilibrium state. This applies both for the folding and the unfolding processes. Cold denaturing thermal unfolding of the proteins is accelerated by negative temperature gradients. Microwave irradiation of the protein solution heated it by about 0.3 degree, and hence the observed acceleration of denaturing is therefore non-thermal.
The alkaline comet assay as described by Olive et al. (Exp. Cell Res. 198, 259-267, 1992) was used to detect DNA damage in cells exposed to low doses (0-5 cGy) of gamma radiation. Experiments were performed using lymphocytes isolated from whole blood of rats. The comet parameters, normalized comet moment and comet length, described by Kent et al. (Int. J. Radiat. Biol. 67, 655-660, 1995), were used as measurements of DNA damage. It was observed that the alkaline comet assay can detect DNA damage at doses as low as 0.6 cGy. The results of the experiments using low-dose gamma radiation are comparable with published results obtained using the alkaline comet assay according to the method of Singh et al. (Int. J. Radiat. Biol. 66, 23-28, 1994). Based on this observation and analysis of results published previously, we conclude that the version of the alkaline comet assay described by Olive et al. is as sensitive as other modifications of the comet assay reported in literature for the detection of DNA damage in cells exposed to low doses of ionizing radiation.
The activity of 0.01-1 microM of melatonin on depolarization-induced 45Ca2+ influx by hypothalamic synaptosomes of rats killed at late evening (2000 h) depended on melatonin preincubation time, exhibiting an early (10 min) stimulation of uptake and an inhibition after 30 min of incubation. Both stimulatory and inhibitory effects were maximal at 2000 h and tended to a minimum at 2400 h, exhibiting intermediate values at 400 h. At 1000 h, only inhibitory effects of melatonin (1 microM) on Ca2+ uptake were found.
The mechanisms of radiation damage production are used to examine the following premises: (1) the number of DNA double-strand breaks per unit dose increases with dose; (2) cell type to cell type variations in yield of DNA dsb per dose occur. Two stages of damage production are identified as possible sources of damage yield modulation; numbers of OH. free radicals reacting with the target, and amount of chemical repair occurring on the target radicals. These factors are discussed in the light of the structures within which cellular DNA is packaged and the known rate constants for the reactions involved. It is concluded from our current knowledge that, in the presence of oxygen: (a) the number of DNA dsb is linearly related to dose, and (b) the yields of DNA damage per dose among cell types are constant. There is a caveat to the latter conclusion: the chromatin structure may be different in radiosensitive cell lines. In the absence of such a difference, variations in radiosensitivity with dose or with cell type are assigned to differences in repair speed and/or accuracy.
Wistar rats were treated in utero on day 16 of gestation either by X-irradiation (1 and 2 Gy), N-ethyl-N-nitrosourea (ENU, 50 mg/kg), or both in combination. The O6-alkylguanine-DNA alkyltransferase (AT) activity of the fetal brain and liver was analyzed and long-term observations were made to reveal any relationship between the O6-ethylguanine repair capability and tumour incidence in the organs of the offspring. The AT activity in the brain was affected to the same extent in the fetuses as in the dams. There was a 60.9% decrease in AT activity in fetuses 24 h after ENU treatment. This correlates with a significant increase in the incidence of brain tumours in the treated offspring (44.1%) compared to control animals. The inductive effect of X-irradiation on AT activity (131.3% for 1 Gy and 201.6% for 2 Gy) corresponded in turn with a reduction of the incidence of tumours after the combined treatment (26.8% and 8.3% tumour incidence, 103.1% and 157.8% AT activity). In the liver of the rat fetuses, there was generally no effect of treatment on AT activity in contrast to the results obtained for the dams, where an increased AT activity (127.70% and 157.4% after X-irradiation, 149.0% and 156.1% after combined treatment) was observed. There were no tumours of the liver observed in the offspring after either treatment alone or after combined treatment. Comparing biochemical and morphological results, it is suggested that X-irradiation of rat fetuses--with relatively low doses--and subsequent treatment with the ethylating carcinogen ENU, could significantly reduce the incidence of brain tumours in adult life. This is possibly a result of the corresponding induction of AT.
The endogenous background level of oxidant-induced DNA damage in vivo has been assayed by measuring 8-hydroxydeoxyguanosine (oh8dG), thymine glycol and thymidine glycol in urine and oh8dG in DNA. The level of oxidative DNA damage as measured by oh8dG in normal rat liver is shown to be extensive (1/130,000 bases in nuclear DNA and 1/8000 bases in mitochondrial DNA), especially in mtDNA. The methylation adduct 7-methylguanine (m7G) has also been found. m7G is one of about 5 adducts found on methylating DNA, and oh8dG is one of about 20 adducts found on oxidizing DNA, e.g., by radiation. We also discuss 3 hitherto unrecognized antioxidants in man.
Progress in identifying the important endogenous processes damaging DNA and developing methods to assay this damage in individuals is presented. This approach may aid studies on modulation of cancer and aging. The endogenous background level of oxidant-induced DNA damage in vivo has been assayed by measuring 8-hydroxydeoxyguanosine (oh8dG), thymine glycol and thymidine glycol in urine and oh8dG in DNA. oh8dG is one of about 20 adducts found on oxidizing DNA, e.g., by radiation. The level of oxidative DNA damage as measured by oh8dG in normal rat liver is shown to be extensive, especially in mtDNA (1/130,000 bases in nuclear DNA and 1/8,000 bases in mitochondrial DNA). We also discuss three hitherto unrecognized antioxidants in man.
There is convincing evidence that cellular prooxidant states--that is, increased concentrations of active oxygen and organic peroxides and radicals--can promote initiated cells to neoplastic growth. Prooxidant states can be caused by different classes of agents, including hyperbaric oxygen, radiation, xenobiotic metabolites and Fenton-type reagents, modulators of the cytochrome P-450 electron-transport chain, peroxisome proliferators, inhibitors of the antioxidant defense, and membrane-active agents. Many of these agents are promoters or complete carcinogens. They cause chromosomal damage by indirect action, but the role of this damage in carcinogenesis remains unclear. Prooxidant states can be prevented or suppressed by the enzymes of the cellular antioxidant defense and low molecular weight scavenger molecules, and many antioxidants are antipromoters and anticarcinogens. Finally, prooxidant states may modulate the expression of a family of prooxidant genes, which are related to cell growth and differentiation, by inducing alterations in DNA structure or by epigenetic mechanisms, for example, by polyadenosine diphosphate-ribosylation of chromosomal proteins.
The ability of fibroblasts to perform unscheduled DNA synthesis (a measure of excision-repair) after UV irradiation was measured radioautographically for seven species at several times after several UV fluences. Both the initial rate and the maximum incorporation of [(3)H]dThd increased with the life-span of the species (shrew, mouse, rat, hamster, cow, elephant, man). Unscheduled DNA synthesis was approximately proportional to the logarithm of life-span.
This review evaluates the applicability of the single cell gel (SCG)/comet assay as a tool for the biomonitoring of individuals accidently, environmentally or occupationally exposed to ionizing radiation. This technique detects single-strand DNA breaks, alkali-labile damage, incomplete excision repair sites and DNA:DNA crosslinking at the level of the individual cell. The advantages of this technique include: (a) data are collected at the level of the individual cell, providing information on the intercellular distribution of damage and repair; (b) only small numbers of cells are required (i.e., only a few thousand); (c) virtually any eukaryotic cell population can be used; and (d) the assay is relatively sensitive (detection limit of 5 cGy gamma rays in human lymphocytes), simple and cost effective. What the assay lacks is specificity for radiation-induced DNA damage. However, the possibility of identifying types of DNA damage specific for ionizing radiation in selected subtypes of cells may be feasible. While additional research is required before the SCG assay can readily be applied as a standard biomonitoring tool for exposure to ionizing radiation, the data collected thus far support a conclusion that such research is clearly warranted.
The potential mutagenic effect of low power microwave at the DNA sequence level in the mouse genome was evaluated by direct DNA analysis. Animals were exposed to microwave at a power density of 1 mW/cm2 for 2 h/day at a frequency of 2.45 GHz over a period of 120, 150 and 200 days. HinfI digested DNA samples from testis and brain of control and exposed animals were hybridized with a synthetic oligo probe (OAT 36) comprising nine repeats of 5'-GACA-3'. As compared to control animals, band patterns in exposed animals were found to be distinctly altered in the range of 7-8 kb which was also substantiated by densitometric analysis. Though the mechanism of this rearrangement is not yet clear, the results obtained at the present dose are of significance. This dose, which has been set as the safe limit for general public exposure by the Non-Ionizing Radiation Committee of the International Radiation Protection Association, may imply a need for (re)evaluation of the mutagenic potential of microwaves at the prescribed safe limit for the personnel and people who are being exposed.
The effects of the inhibitors of topoisomerase I and II, camptothecin and etoposide, as well as novobiocin and adriamycin, on the DNA fragmentation and viability of mouse thymocytes in primary culture were examined. All inhibitors were shown to produce dose-dependent internucleosomal DNA cleavage by resolving isolated DNA by agarose-gel electrophoresis. The DNA fragmentation seemed to precede cell death, determined on the basis of LDH release, by a few hours. Etoposide-induced DNA fragmentation progressively increased after incubation and was enhanced by pretreatment with phorbol 12,13-dibutyrate, a phorbol ester capable of activating protein kinase C, whereas camptothecin-induced DNA fragmentation increased progressively after 12 h incubation and was unaffected by phorbol 12,13-dibutyrate-pretreatment. The process was also energy-dependent and required RNA and protein synthesis and protein phosphorylation, since it was inhibited by sodium azide, actinomycin D, cycloheximide and 1-(5-isoquinoline-sulfonyl)-2-methylpiperazine hydrochloride, a protein kinase inhibitor. DNA fragmentation was also inhibited by zinc ions, suggesting the involvement of a specific endonuclease in DNA cleavage. These phenomena are similar to those detected in thymocytes undergoing apoptosis following exposure to glucocorticoids (Cohen, J.J. and Duke, R.C. (1984) J. Immunol. 132, 38-42). Considering that topoisomerases function in cellular proliferation and differentiation by altering DNA topology, the results suggest that topoisomerases have important roles in T-lymphocyte ontogeny in the thymus and are in part involved in the elimination of autoreactive or harmful cells by an apoptotic process.
Expression of both the DNA repair protein O6-alkylguanine-DNA-alkyltransferase (ATase) and the p53 tumour suppressor protein are inducible by a number of DNA damaging agents. It is probable that DNA strand breaks are the common inducing signals. This similarity, and the function of p53 as a transcription factor lead us to reason that p53 might be involved in ATase inducibility. We now report that the induction of ATase activity in mouse tissues following gamma-radiation is p53 gene dose dependent. While the extent and kinetics of induction in p53 wildtype mice are consistent with previous reports (a 2-3-fold peak increase at 36 h), no induction is observed in p53 null animals. Importantly the heterozygous mice show an intermediate response but the same kinetics. The basal levels of expression in all tissues examined are unaffected by p53 status. These data represent the first report of a discrete DNA repair function being p53 regulated in vivo and their potential clinical implications are discussed.
Two thermophilic and thermostable enzymes, isolated from Sulfolobus solfataricus, S-adenosylhomocysteine hydrolase and 5'-methylthioadenosine phosphorylase, were exposed to 10.4 GHz microwave radiation in order to discriminate between thermal and non-thermal microwave effects. The exposure causes a non-thermal, irreversible and time-dependent inactivation of both enzymes; the inactivation rate is related to the energy absorbed and is independent of the enzyme concentration. The influence of salts on enzyme inactivation has also been investigated. Conformational changes of S-adenosylhomocysteine hydrolase, detected by fluorescence and circular dichroism techniques, suggest that microwaves induce protein structural rearrangements not related to temperature.
In previous research, we have found an increase in DNA single- and double-strand breaks in brain cells of rats after acute exposure (two hours) to a sinusoidal 60-Hz magnetic field. The present experiment was carried out to investigate whether treatment with melatonin and the spin-trap compound N-tert-butyl-alpha-phenylnitrone (PBN) could block the effect of magnetic fields on brain cell DNA. Rats were injected with melatonin (1 mg/kg, sc) or PBN (100 mg/kg, ip) immediately before and after two hours of exposure to a 60-Hz magnetic field at an intensity of 0.5 mT. We found that both drug treatments blocked the magnetic field-induced DNA single- and double-strand breaks in brain cells, as assayed by a microgel electrophoresis method. Since melatonin and PBN are efficient free radical scavengers, these data suggest that free radicals may play a role in magnetic field-induced DNA damage.
Effects of in vivo microwave exposure on DNA strand breaks, a form of DNA damage, were investigated in rat brain cells. In previous research, we have found that acute (2 hours) exposure to pulsed (2 microseconds pulses, 500 pps) 2450-MHz radiofrequency electromagnetic radiation (RFR) (power density 2 mW/cm2, average whole body specific absorption rate 1.2 W/kg) caused an increase in DNA single- and double-strand breaks in brain cells of the rat when assayed 4 hours post exposure using a microgel electrophoresis assay. In the present study, we found that treatment of rats immediately before and after RFR exposure with either melatonin (1 mg/kg/injection, SC) or the spin-trap compound N-tert-butyl-alpha-phenylnitrone (PBN) (100 mg/kg/injection, i.p.) blocks this effects of RFR. Since both melatonin and PBN are efficient free radical scavengers it is hypothesized that free radicals are involved in RFR-induced DNA damage in the brain cells of rats. Since cumulated DNA strand breaks in brain cells can lead to neurodegenerative diseases and cancer and an excess of free radicals in cells has been suggested to be the cause of various human diseases, data from this study could have important implications for the health effects of RFR exposure.
Mouse C3H 10T1/2 fibroblasts and human glioblastoma U87MG cells were exposed to cellular phone communication frequency radiations to investigate whether such exposure produces DNA damage in in vitro cultures. Two types of frequency modulations were studied: frequency-modulated continuous-wave (FMCW), with a carrier frequency of 835.62 MHz, and code-division multiple-access (CDMA) centered on 847.74 MHz. Exponentially growing (U87MG and C3H 10T1/2 cells) and plateau-phase (C3H 10T1/2 cells) cultures were exposed to either FMCW or CDMA radiation for varying periods up to 24 h in specially designed radial transmission lines (RTLs) that provided relatively uniform exposure with a specific absorption rate (SAR) of 0.6 W/kg. Temperatures in the RTLs were monitored continuously and maintained at 37 +/- 0.3 degrees C. Sham exposure of cultures in an RTL (negative control) and 137Cs gamma-irradiated samples (positive control) were included with every experiment. The alkaline comet assay as described by Olive et al. (Exp. Cell Res. 198, 259-269, 1992) was used to measure DNA damage. No significant differences were observed between the test group exposed to FMCW or CDMA radiation and the sham-treated negative controls. Our results indicate that exposure of cultured mammalian cells to cellular phone communication frequencies under these conditions at an SAR of 0.6 W/kg does not cause DNA damage as measured by the alkaline comet assay.
This paper reviews the literature data on the genetic toxicology of radiofrequency (RF) radiation. Whereas in the past most studies were devoted to microwave ovens and radar equipment, it is now mobile telecommunication that attracts most attention. Therefore we focus on mobile telephone frequencies where possible. According to a great majority of the papers, radiofrequency fields, and mobile telephone frequencies in particular, are not genotoxic: they do not induce genetic effects in vitro and in vivo, at least under non-thermal exposure conditions, and do not seem to be teratogenic or to induce cancer. Yet, some investigations gave rather alarming results that should be confirmed and completed by further experiments. Among them the investigation of synergistic effects and of possible mechanisms of action should be emphasised.
Pathological agents such as ionizing radiation and oxidative free radicals can cause breaks in both strands of the DNA at a given site (double-strand break). This is the most serious type of DNA damage because neither strand is able to provide physical integrity or information content, as would be the case for single-strand DNA damage where one strand of the duplex remains intact. The repair of such breaks usually results in an irreversible alteration of the DNA. Two physiological forms of intentional double-strand (ds) DNA breakage and rejoining occur during lymphoid differentiation. One is V(D)J recombination occurring during early B and T cell development, and the other is class switch recombination, occurring exclusively in mature B cells. The manner in which physiological and most pathological double-strand DNA breaks are rejoined to restore chromosomal integrity are the same. Defects during the phases in which pathological or physiological breaks are generated or in which they are joined can result in chromosomal translocations or loss of genetic information at the site of breakage. Such events are the first step in some cancers and may be a key contributor to changes in DNA with age. Inherited defects in this process can result in severe combined immune deficiency. Hence, pathological and physiological DNA double-strand breaks are related to immune defects and cancer and may be one of the key ways in which DNA is damaged during aging.
Work in bioelectromagnetics has long been plagued by problems with replication. This includes experiments done on electromagnetic (EM) field-induced effects in chick embryos. Our laboratory investigated responses of embryos from two flocks of White Leghorn hens. Both flocks were studied simultaneously, and it was found that they responded differently to EM field exposures. Embryos were exposed to 60 Hz, 8 microT EM fields prior to placement in an anoxic chamber. Following re-oxygenation, survival in controls was 34.6%, exposed flock 1 survival was 62% (P < 0.0001) and exposed flock 2 survival was 43% (P < 0.0136). P values are from comparison of data between EM field exposed embryos (flocks 1 and 2) versus controls. In order to induce maximum protection in flock 2, (approximately 62% survival), embryos required a longer exposure time at higher magnetic field strengths. These results reinforce the concepts that genetics are important in determining whether or not chick embryos will respond to EM field stimulation. A broader look at the role of genetic factors emphasizes that these variations in response to external stimuli (e.g., drugs, radiation, and EM fields) are found in all areas of biological research (cell culture, chick, rat, and human studies). The present study suggests that genetics may be a prime cause of the difficulties encountered in replication studies in the field of bioelectromagnetics. We conclude that replication studies should not be undertaken unless care is taken to insure that exactly the same strains of cells or animals are used. Researchers should also first confirm that the responses of their model to non-EM field stimuli are similar to that obtained in the original study.
We have tested an 836.55 MHz field with North American Digital Cellular (NADC) modulation in a 2-year animal bioassay that included fetal exposure. In offspring of pregnant Fischer 344 rats, we tested both spontaneous tumorigenicity and the incidence of induced central nervous system (CNS) tumors after a single dose of the carcinogen ethylnitrosourea (ENU) in utero, followed by intermittent digital-phone field exposure for 24 months. Far-field exposures began on gestational day 19 and continued until weaning at age 21 days. Near-field exposures began at 35 days and continued for the next 22 months, 4 consecutive days weekly, 2 h/day. SAR levels simulated localized peak brain exposures of a cell phone user. Of the 236 original rats, 182 (77%) survived to the termination of the whole experiment and were sacrificed at age 709-712 days. The 54 rats (23%) that died during the study ("preterm rats") formed a separate group for some statistical analyses. There was no evidence of tumorigenic effects in the CNS from exposure to the TDMA field. However, some evidence of tumor-inhibiting effects of TDMA exposure was apparent. Overall, the TDMA field-exposed animals exhibited trends toward a reduced incidence of spontaneous CNS tumors (P < 0. 16, two-tailed) and ENU-induced CNS tumors (P < 0.16, two-tailed). In preterm rats, where primary neural tumors were determined to be the cause of death, fields decreased the incidence of ENU-induced tumors (P < 0.03, two-tailed). We discuss a possible approach to evaluating with greater certainty the possible inhibitory effects of TDMA-field exposure on tumorigenesis in the CNS.
Retinoids, the analogues of vitamin A, have a broad range of effects on different cell types. One biologically active form of vitamin A is all-trans-retinoic acid (ATRA), which binds to retinoic acid receptors, as does its intracellular metabolite, 9-cis-RA. Earlier studies have documented G1 cell cycle arrest and the induction of apoptosis in human adult T-cell leukemia cells after ATRA treatment. Previous work exploring the growth-inhibitory activity of ATRA in human malignancies has implicated several mechanisms that can arrest cells in the G1 phase of the cell cycle, including activation of p21Waf1 and inhibition of cyclin D1 expression. Therefore, we decided to examine the effects of ATRA exposure on G1 cell cycle components in human adult T-cell leukemia cells. Our data demonstrate a correlation between cyclin/cyclin-dependent kinase activity and subunit complex formation with duration of drug exposure. We also observed an increase in p53 protein levels that were not associated with an increase in p21Waf1 levels. Furthermore, we observed a differential effect on cell cycle progression that was temporally related to length of ATRA exposure. These observations, consistent with a bimodal effect of ATRA on cell cycle progression, may have important implications for the clinical application of ATRA.
DNA migration, using single cell gel electrophoresis (comet assay), was studied on brain cells of CBA mice exposed continuously to 50 Hz, 0.5 mT magnetic fields (MF) for 2 hrs, 5 days or 14 days. No differences were observed in the groups MF-exposed for 2 hrs and 5 days compared with controls. However, in the group exposed to MF for 14 days, a significantly extended cell DNA migration was observed (0.02 < p < 0.05). These changes together with results from previous studies indicate that magnetic fields may have genotoxic effects in brain cells.
Human peripheral blood samples collected from three healthy human volunteers were exposed in vitro to pulsed-wave 2450 MHz radiofrequency (RF) radiation for 2 h. The RF radiation was generated with a net forward power of 21 W and transmitted from a standard gain rectangular antenna horn in a vertically downward direction. The average power density at the position of the cells in the flask was 5 mW/cm(2). The mean specific absorption rate, calculated by finite difference time domain analysis, was 2.135 (+/-0.005 SE) W/kg. Aliquots of whole blood that were sham-exposed or exposed in vitro to 50 cGy of ionizing radiation from a (137)Cs gamma-ray source were used as controls. The lymphocytes were examined to determine the extent of primary DNA damage (single-strand breaks and alkali-labile lesions) using the alkaline comet assay with three different slide-processing schedules. The assay was performed on the cells immediately after the exposures and at 4 h after incubation of the exposed blood at 37 +/- 1 degrees C to allow time for rejoining of any strand breaks present immediately after exposure, i.e. to assess the capacity of the lymphocytes to repair this type of DNA damage. At either time, the data indicated no significant differences between RF-radiation- and sham-exposed lymphocytes with respect to the comet tail length, fluorescence intensity of the migrated DNA in the tail, and tail moment. The conclusions were similar for each of the three different comet assay slide-processing schedules examined. In contrast, the response of lymphocytes exposed to ionizing radiation was significantly different from RF-radiation- and sham-exposed cells. Thus, under the experimental conditions tested, there is no evidence for induction of DNA single-strand breaks and alkali-labile lesions in human blood lymphocytes exposed in vitro to pulsed-wave 2450 MHz radiofrequency radiation, either immediately or at 4 h after exposure.