The spatial distributions of induced 27 or 2450 MHz radiofrequency (RF) electric fields (E-fields) and specific absorption rates (SARs) in a three-component spherical cell model (cytoplasm, membrane, extracellular space) were determined by Mie scattering theory. The results were compared to results for the same cell model but with 0.5 nm thick of bound water on the inner (cytoplasmic) and outer (extracellular) membrane surfaces (i.e., five-component cell model). The results provide insight regarding direct frequency-dependent RF radiation effects at the cellular level. Induced E-fields and SARs were calculated for two bound-water characteristic frequencies (400 or 1000 MHz) and ionic conductivities (1-1000 mS/m). In order to estimate the dependence of the results on bound water within the membrane per se, the model was revised to include bound water within the inner and outer membrane surfaces. The results were as follows: 1) on the x-axis, the y- and z-components of the induced E-field were of insignificant magnitude compared to the x-component for an incident E-field parallel to the x-axis; 2) the ratio of transmembrane E-fields induced by 2450 MHz vs. 27 MHz RF [i.e., Ex (2450 MHz)/Ex (27 MHz)] was 0.1; 3) for the three-component cell model, the corresponding SAR ratios [SAR (2450 MHz)/SAR (27MHz)] in the cytoplasm and extracellular space were 1.66 and 5.0, respectively; 4) the SAR rations [SAR (2450 MHz)/SAR (27 MHz)] for the cytoplasm and extracellular space for the five-component cell model were 1.66 and 5.0, respectively; 5) the ratio of the E-fields induced in the cytoplasmic and extracellular layers of bound water in the five-component cell model [E (2450 MHz)/ E (27Mhz)] were 0.62 and 0.63, respectively; 6) the SAR ratios [SAR (2450 MHz)/SAR (27 MHz)] for the cytoplasmic and extracellular bound-water layers were 66 and 65.3, respectively; and 7) variation of bound-water characteristic frequency, ionic conductivity, or bound-water incorporation inside the membrane surfaces, per se, did not significantly affect the E-field or SAR ratios. These results indicate that frequency-dependent nonuniformities may occur in the distribution of induced RF E-fields and SARs at the cellular level.
Previous in vitro studies provide evidence that RF electromagnetic radiation modulates proliferation of human glioma, lymphocytes, and other cell types. The mechanism of RF radiation cell proliferation modulation, as well as mechanisms for effects on other cell physiologic endpoints, are not well understood. To obtain insight regarding interaction mechanisms, we investigated effects of RF radiation exposure on interleukin 2 (IL-2) -dependent proliferation of cytolytic T lymphocytes (CTLL-2). After exposure to RF radiation in the presence or absence of IL-2 cells were cultured at various physiological concentrations of IL-2. Treatment effects on CTLL-2 proliferation were determined by tritiated thymidine incorporation immediately or 24 h after exposure. Exposure to 2450 MHz RIF radiation at specific absorption rates (SARs) of greater than 25 W/kg (induced E-field strength 98.4 V/m) induced a consistent, statistically significant reduction in CTLL-2 proliferation, especially at low IL-2 concentrations. At lower SARs, 2450 MHz exposure increased CTLL-2 proliferation immediately after exposure but reduced 24 h postexposure proliferation. RF radiation effects depended on the mitotic state of the cells at the time of exposure. Comparison of the effects of temperature elevation and RF radiation indicated significant qualitative and quantitative differences.
The induction of stress proteins in HeLa and CHO cells was investigated following a 2 h exposure to radiofrequency (RF) or microwave radiation. Cells were exposed or sham exposed in vitro under isothermal (37 ± 0.2 °C) conditions. HeLa cells were exposed to 27‐ or 2450 MHz continuous wave (CW) radiation at a specific absorption rate (SAR) of 25 W/kg. CHO cells were exposed to CW 27 MHz radiation at a SAR of 100 W/kg. Parallel positive control studies included 2 h exposure of HeLa or CHO cells to 40 °C or to 45 μM cadmium sulfate. Stress protein induction was assayed 24 h after treatment by electrophoresis of whole‐cell extracted protein labeled with [35S]‐methionine. Both cell types exhibited well‐characterized responses to the positive control stresses. Under these exposure conditions, neither microwave nor RF radiation had a detectable effect on stress protein induction as determined by either comparison of RF‐exposed cells with sham‐exposed cells or comparison with heat‐stressed or Cd++ positive control cells. Bioelectromagnetics 18:499–505, 1997. © 1997 Wiley‐Liss, Inc.
Isothermal (37 +/- 0.2 degrees C) exposure of glioma cells (LN71) for 2 h to 27 or 2450 MHz continuous-wave radiofrequency (RF) radiation in vitro modulated the rates of DNA and RNA synthesis 1, 3, and 5 days after exposure. The alterations indicate effects on cell proliferation and were not caused by RF-induced cell heating. The dose response for either frequency of the radiation was biphasic. Exposure to specific absorption rates (SARs) of 50 W/kg or less stimulated incorporation rates of tritiated thymidine (3H-TdR) and tritiated uridine (3H-UdR), whereas higher SARs suppressed DNA and RNA synthesis. Statistically significant time-dependent alterations were detected for up to 5 days postexposure, suggesting a kinetic cellular response to RF radiation and the possibility of cumulative effects on cell proliferation. General mechanisms of effects are discussed.
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