DNA damage in human leukocytes after acute in vitro exposure to a 1.9 GHz pulse-modulated radiofrequency field

Blood cultures from human volunteers were exposed to an acute 1.9 GHz pulse-modulated radiofrequency (RF) field for 2 h using a series of six circularly polarized, cylindrical waveguides. Mean specific absorption rates (SARs) ranged from 0 to 10 W/kg, and the temperature within the cultures during the exposure was maintained at 37.0 +/- 0.5 degrees C. DNA damage was quantified in leukocytes by the alkaline comet assay and the cytokinesis-block micronucleus assay. When compared to the sham-treated controls, no evidence of increased primary DNA damage was detected by any parameter for any of the RF-field-exposed cultures when evaluated using the alkaline comet assay. Furthermore, no significant differences in the frequency of binucleated cells, incidence of micronucleated binucleated cells, or total incidence of micronuclei were detected between any of the RF-field-exposed cultures and the sham-treated control at any SAR tested. These results do not support the hypothesis that acute, nonthermalizing 1.9 GHz pulse-modulated RF-field exposure causes DNA damage in cultured human leukocytes.     

Effects of modulated microwave radiation at cellular telephone frequency (1.95 GHz) on X-ray-induced chromosome aberrations in human lymphocytes in vitro

The case for a DNA-damaging action produced by radiofrequency (RF) signals remains controversial despite extensive research. With the advent of the Universal Mobile Telecommunication System (UMTS) the number of RF-radiation-exposed individuals is likely to escalate. Since the epigenetic effects of RF radiation are poorly understood and since the potential modifications of repair efficiency after exposure to known cytotoxic agents such as ionizing radiation have been investigated infrequently thus far, we studied the influence of UMTS exposure on the yield of chromosome aberrations induced by X rays. Human peripheral blood lymphocytes were exposed in vitro to a UMTS signal (frequency carrier of 1.95 GHz) for 24 h at 0.5 and 2.0 W/kg specific absorption rate (SAR) using a previously characterized waveguide system. The frequency of chromosome aberrations was measured on metaphase spreads from cells given 4 Gy of X rays immediately before RF radiation or sham exposures by fluorescence in situ hybridization. Unirradiated controls were RF-radiation- or sham-exposed. No significant variations due to the UMTS exposure were found in the fraction of aberrant cells. However, the frequency of exchanges per cell was affected by the SAR, showing a small but statistically significant increase of 0.11 exchange per cell compared to 0 W/kg SAR. We conclude that, although the 1.95 GHz signal (UMTS modulated) does not exacerbate the yield of aberrant cells caused by ionizing radiation, the overall burden of X-ray-induced chromosomal damage per cell in first-mitosis lymphocytes may be enhanced at 2.0 W/kg SAR. Hence the SAR may either influence the repair of X-ray-induced DNA breaks or alter the cell death pathways of the damage response.     

TP53 tumor suppressor protein in normal human fibroblasts does not respond to 837 MHz microwave exposure.

The TP53 tumor suppressor protein (formerly known as p53) responds to a wide variety of environmental insults. To evaluate the safety of cellular telephones, TP53 responses in human fibroblast cells were studied after exposure to 837 MHz microwaves. Cells were exposed in a temperature-controlled transverse electromagnetic (TEM) chamber to a specific absorption rate (SAR) of 0.9 or 9.0 W/kg at 837 MHz continuous-wave (CW) microwave irradiation for 2 h. The TP53 protein levels were measured by Western blot at 2, 8, 24 and 48 h after treatment. The TP53 protein levels in microwave-treated cells, sham-treated cells, and untreated cells remained unchanged relative to each other at all times tested (Fisher test and Student-Newman-Keuls test, P > 0.05). No morphological alterations were observed in microwave-treated cells compared to sham-treated cells. We conclude that TP53 protein expression levels in cultured human fibroblast cells do not change significantly during a 48-h period after exposure to 837 MHz continuous microwaves for 2 h at SAR levels of 0.9 or 9.0 W/kg.     

Effect of radiofrequency electromagnetic field exposure on in vitro models of neurodegenerative disease

In this work we tested viability, proliferation, and vulnerability of neural cells, after continuous radiofrequency (RF) electromagnetic fields exposure (global system for mobile telecommunications (GSM) modulated 900 MHz signal at a specific absorption rate (SAR) of 1 W/kg and maximum duration 144 h) generated by transverse electromagnetic cells. We used two cellular systems, SN56 cholinergic for example, SN56 cholinergic cell line and rat primary cortical neurons, and well‐known neurotoxic challenges, such as glutamate, 25‐35AA beta‐amyloid, and hydrogen peroxide. Exposure to RF did not change viability/proliferation rate of the SN56 cholinergic cells or viability of cortical neurons. Co‐exposure to RF exacerbated neurotoxic effect of hydrogen peroxide in SN56, but not in primary cortical neurons, whereas no cooperative effects of RF with glutamate and 25‐35AA beta‐amyloid were found. These data suggest that only under particular circumstances exposure to GSM modulated, 900 MHz signal act as a co‐stressor for oxidative damage of neural cells. Bioelectromagnetics 30:564–572, 2009. © 2009 Wiley‐Liss, Inc.     

Chromosome damage and micronucleus formation in human blood lymphocytes exposed in vitro to radiofrequency radiation at a cellular telephone frequency (847.74 MHz, CDMA)

Peripheral blood samples collected from four healthy nonsmoking human volunteers were diluted with tissue culture medium and exposed in vitro for 24 h to 847.74 MHz radiofrequency (RF) radiation (continuous wave), a frequency employed for cellular telephone communications. A code division multiple access (CDMA) technology was used with a nominal net forward power of 75 W and a nominal power density of 950 W/m(2) (95 mW/cm(2)). The mean specific absorption rate (SAR) was 4.9 or 5.5 W/kg. Blood aliquots that were sham-exposed or exposed in vitro to an acute dose of 1.5 Gy of gamma radiation were included in the study as controls. The temperatures of the medium during RF-radiation and sham exposures in the Radial Transmission Line facility were controlled at 37 +/- 0.3 degrees C. Immediately after the exposures, lymphocytes were cultured at 37 +/- 1 degrees C for 48 or 72 h. The extent of genetic damage was assessed from the incidence of chromosome aberrations and micronuclei. The kinetics of cell proliferation was determined from the mitotic indices in 48-h cultures and from the incidence of binucleate cells in 72-h cultures. The data indicated no significant differences between RF-radiation-exposed and sham-exposed lymphocytes with respect to mitotic indices, frequencies of exchange aberrations, excess fragments, binucleate cells, and micronuclei. The response of gamma-irradiated lymphocytes was significantly different from that of both RF-radiation-exposed and sham-exposed cells for all of these indices. Thus there was no evidence for induction of chromosome aberrations and micronuclei in human blood lymphocytes exposed in vitro for 24 h to 847.74 MHz RF radiation (CDMA) at SARs of 4.9 or 5.5 W/kg.     

Development of a rat head exposure system for simulating human exposure to RF fields from handheld wireless telephones

The aim of this project was to develop an animal exposure system for the biological effect studies of radio frequency fields from handheld wireless telephones, with energy deposition in animal brains comparable to those in humans. The finite‐difference time‐domain (FDTD) method was initially used to compute specific absorption rate (SAR) in an ellipsoidal rat model exposed with various size loop antennas at different distances from the model. A 3 × 1 cm rectangular loop produced acceptable SAR patterns. A numerical rat model based on CT images was developed by curve‐fitting Hounsfield Units of CT image pixels to tissue dielectric properties and densities. To design a loop for operating at high power levels, energy coupling and impedance matching were optimized using capacitively coupled feed lines embedded in a Teflon rod. Sprague Dawley rats were exposed with the 3 × 1 cm loop antennas, tuned to 837 or 1957 MHz for thermographically determined SAR distributions. Point SARs in brains of restrained rats were also determined thermometrically using fiberoptic probes. Calculated and measured SAR patterns and results from the various exposure configurations are in general agreement. The FDTD computed average brain SAR and ratio of head to whole body absorption were 23.8 W/kg/W and 62% at 837 MHz, and 22.6 W/kg/W and 89% at 1957 MHz. The average brain to whole body SAR ratio was 20 to 1 for both frequencies. At 837 MHz, the maximum measured SAR in the restrained rat brains was 51 W/kg/W in the cerebellum and 40 W/kg/W at the top of the cerebrum. An exposure system operating at 837 MHz is ready for in vivo biological effect studies of radio frequency fields from portable cellular telephones. Two‐tenths of a watt input power to the loop antenna will produce 10 W/kg maximum SAR, and an estimated 4.8 W/kg average brain SAR in a 300 g medium size rat. Bioelectromagnetics 20:75–92, 1999. © 1999 Wiley‐Liss, Inc.     

Combined effects of 872 MHz radiofrequency radiation and ferrous chloride on reactive oxygen species production and DNA damage in human SH‐SY5Y neuroblastoma cells

The aim of the present study was to investigate possible cooperative effects of radiofrequency (RF) radiation and ferrous chloride (FeCl₂) on reactive oxygen species (ROS) production and DNA damage. In order to test intracellular ROS production as a possible underlying mechanism of DNA damage, we applied the fluorescent probe DCFH‐DA. Integrity of DNA was quantified by alkaline comet assay. The exposures to 872 MHz RF radiation were conducted at a specific absorption rate (SAR) of 5 W/kg using continuous waves (CW) or a modulated signal similar to that used in Global System for Mobile Communications (GSM) phones. Four groups were included: (1) Sham exposure (control), (2) RF radiation, (3) Chemical treatment, (4) Chemical treatment, and RF radiation. In the ROS production experiments, human neuroblastoma (SH‐SY5Y) cells were exposed to RF radiation and 10 µg/ml FeCl₂ for 1 h. In the comet assay experiments, the exposure time was 3 h and an additional chemical (0.015% diethyl maleate) was used to make DNA damage level observable. The chemical treatments resulted in statistically significant responses, but no effects from either CW or modulated RF radiation were observed on ROS production, DNA damage or cell viability. Bioelectromagnetics 31:417–424, 2010. © 2010 Wiley‐Liss, Inc.     

Phosphorylation and gene expression of p53 are not affected in human cells exposed to 2.1425 GHz band CW or W-CDMA modulated radiation allocated to mobile radio base stations

A large-scale in vitro study focusing on low-level radiofrequency (RF) fields from mobile radio base stations employing the International Mobile Telecommunication 2000 (IMT-2000) cellular system was conducted to test the hypothesis that modulated RF fields induce apoptosis or other cellular stress response that activate p53 or the p53-signaling pathway. First, we evaluated the response of human cells to microwave exposure at a specific absorption rate (SAR) of 80 mW/kg, which corresponds to the limit of the average whole-body SAR for general public exposure defined as a basic restriction by the International Commission on Non-Ionizing Radiation Protection (ICNIRP) guidelines. Second, we investigated whether continuous wave (CW) and wideband code division multiple access (W-CDMA) modulated signal RF fields at 2.1425 GHz induced apoptosis or any signs of stress. Human glioblastoma A172 cells were exposed to W-CDMA radiation at SARs of 80, 250, and 800 mW/kg, and CW radiation at 80 mW/kg for 24 or 48 h. Human IMR-90 fibroblasts from fetal lungs were exposed to both W-CDMA and CW radiation at a SAR of 80 mW/kg for 28 h. Under the RF field exposure conditions described above, no significant differences in the percentage of apoptotic cells were observed between the test groups exposed to RF signals and the sham-exposed negative controls, as evaluated by the Annexin V affinity assay. No significant differences in expression levels of phosphorylated p53 at serine 15 or total p53 were observed between the test groups and the negative controls by the bead-based multiplex assay. Moreover, microarray hybridization and real-time RT-PCR analysis showed no noticeable differences in gene expression of the subsequent downstream targets of p53 signaling involved in apoptosis between the test groups and the negative controls. Our results confirm that exposure to low-level RF signals up to 800 mW/kg does not induce p53-dependent apoptosis, DNA damage, or other stress response in human cells.     

The effect of exposure to radiofrequency LTE signal and coexposure to mitomycin-C in Chinese hamster lung fibroblast V79 cells

This study aims to investigate the cellular effects of radiofrequency exposure, 1950 MHz, long-term evolution (LTE) signal, administered alone and in combination with mitomycin-C (MMC), a well-known cytotoxic agent. Chinese hamster lung fibroblast (V79) cells were exposed/sham exposed in a waveguide-based system under strictly controlled conditions of both electromagnetic and environmental parameters, at specific absorption rate (SAR) of 0.3 and 1.25 W/kg. Chromosomal damage (micronuclei formation), oxidative stress (reactive oxygen species [ROS] formation), and cell cycle progression were analyzed after exposure and coexposure. No differences between exposed samples and sham-controls were detected following radiofrequency exposure alone, for all the experimental conditions tested and biological endpoints investigated. When radiofrequency exposure was followed by MMC treatment, 3 h pre-exposure did not modify MMC-induced micronuclei. Pre-exposure of 20 h at 0.3 W/kg did not modify the number of micronuclei induced by MMC, while 1.25 W/kg resulted in a significant reduction of MMC-induced damage. Absence of effects was also detected when CW was used, at both SAR levels. MMC-induced ROS formation resulted significantly decreased at both SAR levels investigated, while cell proliferation and cell cycle progression were not affected by coexposures. The results here reported provide no evidence of direct effects of 1950 MHz, LTE signal. Moreover, they further support our previous findings on the capability of radiofrequency pre-exposure to induce protection from a subsequent toxic treatment, and the key role of the modulated signals and the experimental conditions adopted in eliciting the effect.     

Effects of 837 and 1950 MHz radiofrequency radiation exposure alone or combined on oxidative stress in MCF10A cells

The aim of this study was to determine whether the exposure to either single or multiple radio‐frequency (RF) radiation frequencies could induce oxidative stress in cell cultures. Exposures of human MCF10A mammary epithelial cells to either a single frequency (837 MHz alone or 1950 MHz alone) or multiple frequencies (837 and 1950 MHz) were conducted at specific absorption rate (SAR) values of 4 W/kg for 2 h. During the exposure period, the temperature in the exposure chamber was maintained isothermally. Intracellular levels of reactive oxygen species (ROS), the antioxidant enzyme activity of superoxide dismutase (SOD), and the ratio of reduced/oxidized glutathione (GSH/GSSG) showed no statistically significant alterations as the result of either single or multiple RF radiation exposures. In contrast, ionizing radiation‐exposed cells, used as a positive control, showed evident changes in all measured biological endpoints. These results indicate that single or multiple RF radiation exposure did not elicit oxidative stress in MCF10A cells under our exposure conditions. Bioelectromagnetics 33:604–611, 2012. © 2012 Wiley Periodicals, Inc.     

Acute radio frequency irradiation does not affect cell cycle, cellular migration, and invasion

Although in vitro studies have been previously conducted to determine the biological effects of radio frequency (RF) radiation, it has not yet been determined whether or not RF radiation poses a potential hazard. This study was conducted to determine whether RF radiation exposure exerts detectable effects on cell cycle distribution, cellular invasion, and migration. NIH3T3 mouse fibroblasts were exposed to 849 MHz of RF radiation at average SAR values of 2 or 10 W/kg for either 1 h, or for 1 h per day for 3 days. During the exposure period, the temperature in the exposure chamber was maintained isothermally by circulating water throughout the cavity. Cell cycle distribution was analyzed at 24 and 48 h after exposure, by flow cytometry. We detected no statistically significant differences between the sham-exposed and RF radiation-exposed cells. Cellular invasion and migration were assessed by in vitro Matrigel invasion and Transwell migration assays. The RF radiation-exposed groups evidenced no significant changes in motility and invasiveness compared to the sham-exposed group. However, the ionizing radiation-exposed cells, used as a positive control group, manifested dramatic alterations in their cell cycle distribution, cellular invasiveness, and migration characteristics. Our results show that 849 MHz RF radiation exposure exerts no detectable effects on cell cycle distribution, cellular migration, or invasion at average SAR values of 2 or 10 W/kg.     

Induction of an adaptive response in human blood lymphocytes exposed to radiofrequency fields: influence of the universal mobile telecommunication system (UMTS) signal and the specific absorption rate

The induction of an adaptive response (AR) was examined in human peripheral blood lymphocytes exposed to non-ionizing radiofrequency fields (RF). Cells from nine healthy human volunteers were stimulated for 24h with phytohaemagglutinin and then exposed for 20h to an adaptive dose (AD) of a 1950MHz RF UMTS (universal mobile telecommunication system) signal used for mobile communications, at different specific absorption rates (SAR) of 1.25, 0.6, 0.3, and 0.15W/kg. This was followed by treatment of the cells at 48h with a challenge dose (CD) of 100ng/ml mitomycin C (MMC). Lymphocytes were collected at the end of the 72h total culture period. The cytokinesis-block method was used to record the frequency of micronuclei (MN) as genotoxicity end-point. When lymphocytes from six donors were pre-exposed to RF at 0.3W/kg SAR and then treated with MMC, these cells showed a significant reduction in the frequency of MN, compared with the cells treated with MMC alone; this result is indicative of induction of AR. The results from our earlier study indicated that lymphocytes that were stimulated for 24h, exposed for 20h to a 900MHz RF GSM (global system for mobile communication) signal at 1.25W/kg SAR and then treated with 100ng/ml MMC, also exhibited AR. These overall data suggest that the induction of AR depends on RF frequency, type of the signal and SAR. Further characterization of RF-induced AR is in progress.     

Evaluation of genotoxic effects in human leukocytes after in vitro exposure to 1950 MHz UMTS radiofrequency field

In the present study the third generation wireless technology of the Universal Mobile Telecommunication System (UMTS) signal was investigated for the induction of genotoxic effects in human leukocytes. Peripheral blood from six healthy donors was used and, for each donor, intermittent exposures (6 min RF on, 2 h RF off) at the frequency of 1950 MHz were conducted at a specific absorption rate of 2.2 W/kg. The exposures were performed in a transverse electro magnetic (TEM) cell hosted in an incubator under strictly controlled conditions of temperature and dosimetry. Following long duration intermittent RF exposures (from 24 to 68 h) in different stages of the cell cycle, micronucleus formation was evaluated by applying the cytokinesis block micronucleus assay, which also provides information on cell division kinetics. Primary DNA damage (strand breaks/alkali labile sites) was also investigated following 24 h of intermittent RF exposures, by applying the alkaline single cell gel electrophoresis (SCG)/comet assay. Positive controls were included by treating cell cultures with Mitomycin-C and methylmethanesulfonate for micronucleus and comet assays, respectively. The results obtained indicate that intermittent exposures of human lymphocytes in different stages of cell cycle do not induce either an increase in micronucleated cells, or change in cell cycle kinetics; moreover, 24 h intermittent exposures also fail to affect DNA structure of human leukocytes soon after the exposures, likely indicating that repairable DNA damage was not induced.     

DNA synthesis and cell proliferation in C6 glioma and primary glial cells exposed to a 836.55 MHz modulated radiofrequency field

We have tested the hypothesis that modulated radiofrequency (RF) fields may act as a tumor-promoting agent by altering DNA synthesis, leading to increased cell proliferation. In vitro tissue cultures of transformed and normal rat glial cells were exposed to an 836.55 MHz, packet-modulated RF field at three power densities: 0.09, 0.9, and 9 mW/cm², resulting in specific absorption rates (SARs) ranging from 0.15 to 59 μW/g. TEM-mode transmission-line cells were powered by a prototype time-domain multiple-access (TDMA) transmitter that conforms to the North American digital cellular telephone standard. One sham and one energized TEM cell were placed in standard incubators maintained at 37 °C and 5% CO₂. DNA synthesis experiments at 0.59–59 μW/g SAR were performed on log-phase and serum-starved semiquiescent cultures after 24 h exposure. Cell growth at 0.15–15 μW/g SAR was determined by cell counts of log-phase cultures on days 0, 1, 5, 7, 9, 12, and 14 of a 2 week protocol. Results from the DNA synthesis assays differed for the two cell types. Sham-exposed and RF-exposed cultures of primary rat glial cells showed no significant differences for either log-phase or serum-starved condition. C₆ glioma cells exposed to RF at 5.9 μW/g SAR (0.9 mW/cm²) exhibited small (20–40%) significant increases in 38% of [³H]thymidine incorporation experiments. Growth curves of sham and RF-exposed cultures showed no differences in either normal or transformed glial cells at any of the power densities tested. Cell doubling times of C₆ glioma cells [sham (21.9 ± 1.4 h) vs. field (22.7 ± 3.2 h)] also demonstrated no significant differences that could be attributed to altered DNA synthesis rates. Under these conditions, this modulated RF field did not increase cell proliferation of normal or transformed cultures of glial origin. Bioelectromagnetics 18:230–236, 1997. © 1997 Wiley-Liss, Inc.     

Role of modulation on the effect of microwaves on ornithine decarboxylase activity in L929 cells

The effect of 835 MHz microwaves on the activity of ornithine decarboxylase (ODC) in L929 murine cells was investigated at an SAR of ∼2.5 W/kg. The results depended upon the type of modulation employed. AM frequencies of 16 Hz and 60 Hz produced a transient increase in ODC activity that reached a peak at 8 h of exposure and returned to control levels after 24 h of exposure. In this case, ODC was increased by a maximum of 90% relative to control levels. A 40% increase in ODC activity was also observed after 8 h of exposure with a typical signal from a TDMA digital cellular telephone operating in the middle of its transmission frequency range (∼840 MHz). This signal was burst modulated at 50 Hz, with approximately 30% duty cycle. By contrast, 8 h exposure with 835 MHz microwaves amplitude modulated with speech produced no significant change in ODC activity. Further investigations, with 8 h of exposure to AM microwaves, as a function of modulation frequency, revealed that the response is frequency dependent, decreasing sharply at 6 Hz and 600 Hz. Exposure with 835 MHz microwaves, frequency modulated with a 60 Hz sinusoid, yielded no significant enhancement in ODC activity for exposure times ranging between 2 and 24 h. Similarly, exposure with a typical signal from an AMPS analog cellular telephone, which uses a form of frequency modulation, produced no significant enhancement in ODC activity. Exposure with 835 MHz continuous wave microwaves produced no effects for exposure times between 2 and 24 h, except for a small but statistically significant enhancement in ODC activity after 6 h of exposure. Comparison of these results suggests that effects are much more robust when the modulation causes low-frequency periodic changes in the amplitude of the microwave carrier. Bioelectromagnetics 18:132–141, 1997. © 1997 Wiley-Liss, Inc.     

Effects of combined radiofrequency radiation exposure on the cell cycle and its regulatory proteins

The aim of this study was to investigate whether single or combined radio frequency (RF) radiation exposure has effects on the cell cycle and its regulatory proteins. Exposure of MCF7 cells to either single (837 MHz) or combined (837 and 1950 MHz) RF radiation was conducted at specific absorption rate values of 4 W/kg for 1 h. During the exposure period, the chamber was made isothermal by circulating water through the cavity. After RF radiation exposure, DNA synthesis rate and cell cycle distribution were assessed. The levels of cell cycle regulatory proteins, p53, p21, cyclins, and cyclin‐dependent kinases were also examined. The positive control group was exposed to 0.5 and 4 Gy doses of ionizing radiation (IR) and showed changes in DNA synthesis and cell cycle distribution. The levels of p53, p21, cyclin A, cyclin B1, and cyclin D1 were also affected by IR exposure. In contrast to the IR‐exposed group, neither the single RF radiation‐ nor the combined RF radiation‐exposed group elicited alterations in DNA synthesis, cell cycle distribution, and levels of cell cycle regulatory proteins. These results indicate that neither single nor combined RF radiation affect cell cycle progression. Bioelectromagnetics 32:169–178, 2011. © 2010 Wiley‐Liss, Inc.     

Effects of exposure to a 1950 MHz radio frequency field on expression of Hsp70 and Hsp27 in human glioma cells

Human glioma MO54 cells were used to investigate whether radio frequency (RF) field exposure could activate stress response genes. Cells were exposed to continuous wave 1950 MHz or sham conditions for up to 2 h. Specific absorption rates (SARs) were 1, 2, and 10 W/kg. For the cell growth experiment, cell numbers were counted at 0-4 days after exposure. Expression of Hsp27 and Hsp70, as well as the level of phosphorylated Hsp27 (78Ser) protein, was determined by Western blotting. It was found that sham exposed and RF exposed cells demonstrated a similar growth pattern up to 4 days after RF field exposure. RF field exposure at both 2 and 10 W/kg did not affect the growth of MO54 cells. In addition, there were no significant differences in protein expression of Hsp27 and Hsp70 between sham exposed and RF exposed cells at a SAR of 1, 2, or 10 W/kg for 1 and 2 h. However, exposure to RF field at a SAR of 10 W/kg for 1 and 2 h decreased the protein level of phosphorylated Hsp27 (78Ser) significantly. Our results suggest that although exposure to a 1950 MHz RF field has no effect on cell proliferation and expression of Hsp 27 and Hsp70, it may inhibit the phosphorylation of Hsp27 at Serine 78 in MO54 cells.     

DNA damage and micronucleus induction in human leukocytes after acute in vitro exposure to a 1.9 GHz continuous-wave radiofrequency field

Human blood cultures were exposed to a 1.9 GHz continuous-wave (CW) radiofrequency (RF) field for 2 h using a series of six circularly polarized, cylindrical waveguides. Mean specific absorption rates (SARs) of 0.0, 0.1, 0.26, 0.92, 2.4 and 10 W/kg were achieved, and the temperature within the cultures during a 2-h exposure was maintained at 37.0 +/- 0.5 degrees C. Concurrent negative (incubator) and positive (1.5 Gy (137)Cs gamma radiation) control cultures were run for each experiment. DNA damage was quantified immediately after RF-field exposure using the alkaline comet assay, and four parameters (tail ratio, tail moment, comet length and tail length) were used to assess DNA damage for each comet. No evidence of increased primary DNA damage was detected by any parameter for RF-field-exposed cultures at any SAR tested. The formation of micronuclei in the RF-field-exposed blood cell cultures was assessed using the cytokinesis-block micronucleus assay. There was no significant difference in the binucleated cell frequency, incidence of micronucleated binucleated cells, or total incidence of micronuclei between any of the RF-field-exposed cultures and the sham-exposed controls at any SAR tested. These results do not support the hypothesis that acute, nonthermalizing 1.9 GHz CW RF-field exposure causes DNA damage in cultured human leukocytes.     

Measurement of DNA damage and apoptosis in Molt-4 cells after in vitro exposure to radiofrequency radiation

To determine whether exposure to radiofrequency (RF) radiation can induce DNA damage or apoptosis, Molt-4 T lymphoblastoid cells were exposed with RF fields at frequencies and modulations of the type used by wireless communication devices. Four types of frequency/modulation forms were studied: 847.74 MHz code-division multiple-access (CDMA), 835.62 MHz frequency-division multiple-access (FDMA), 813.56 MHz iDEN(R) (iDEN), and 836.55 MHz time-division multiple-access (TDMA). Exponentially growing cells were exposed to RF radiation for periods up to 24 h using a radial transmission line (RTL) exposure system. The specific absorption rates used were 3.2 W/kg for CDMA and FDMA, 2.4 or 24 mW/kg for iDEN, and 2.6 or 26 mW/kg for TDMA. The temperature in the RTLs was maintained at 37 degrees C +/- 0.3 degrees C. DNA damage was measured using the single-cell gel electrophoresis assay. The annexin V affinity assay was used to detect apoptosis. No statistically significant difference in the level of DNA damage or apoptosis was observed between sham-treated cells and cells exposed to RF radiation for any frequency, modulation or exposure time. Our results show that exposure of Molt-4 cells to CDMA, FDMA, iDEN or TDMA modulated RF radiation does not induce alterations in level of DNA damage or induce apoptosis.     

Effects of continuous and intermittent exposure to RF fields with a wide range of SARs on cell growth, survival, and cell cycle distribution

To examine the biological effects of radio frequency (RF) electromagnetic fields in vitro, we have examined the fundamental cellular responses, such as cell growth, survival, and cell cycle distribution, following exposure to a wide range of specific absorption rates (SAR). Furthermore, we compared the effects of continuous and intermittent exposure at high SARs. An RF electromagnetic field exposure unit operating at a frequency of 2.45 GHz was used to expose cells to SARs from 0.05 to 1500 W/kg. When cells were exposed to a continuous RF field at SARs from 0.05 to 100 W/kg for 2 h, cellular growth rate, survival, and cell cycle distribution were not affected. At 200 W/kg, the cell growth rate was suppressed and cell survival decreased. When the cells were exposed to an intermittent RF field at 300 W/kg(pk), 900 W/kg(pk) and 1500 W/kg(pk) (100 W/kg(mean)), no significant differences were observed between these conditions and intermittent wave exposure at 100 W/kg. When cells were exposed to a SAR of 50 W/kg for 2 h, the temperature of the medium around cells rose to 39.1 degrees C, 100 W/kg exposure increased the temperature to 41.0 degrees C, and 200 W/kg exposure increased the temperature to 44.1 degrees C. Exposure to RF radiation results in heating of the medium, and the thermal effect depends on the mean SAR. Hence, these results suggest that the proliferation disorder is caused by the thermal effect.