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(Database last updated on Mar 27, 2024)
| ID Number | 1606 | |
| Study Type | In Vivo | |
| Model | In vivo studies in Spain on seizures, hormonal glands (thyroid and thymus) and heat-shock proteins in rats and humans exposed to microwaves/mobile phone emissions plus in vitro studies. | |
| Details | Sprague Dawley rats (n = 4 groups of 8 rats) +/- treatment with picrotoxin (to induce seizures) were exposed to 900 MHz (GSM) for 1 hr in a restraining tube exposure apparatus. FDTD modeling indicated an average whole body SAR of 0.15-0.24 W/kg and a brain exposure of 0.27-0.42 W/kg (average), 0.31-0.47 (peak). One week before exposure, some rats were anesthetized and screws installed over the frontal and occipital cortices to function as electrodes for EEG to monitor seizure activity. Following exposure, brains were removed and prepared for in situ hybridization to determine c-Fos levels in the cerebral cortex, hippocampus, and thalamus. The authors report that RF exposure alone did not affect seizures or c-Fos expression. However after only 5 minutes of RF exposure in picrotoxin-treated rats, the animals experienced muscle twitches followed by 20-30 minutes of (with the exception of 2 animals) of intermittent seizures. Picrotoxin treatment alone resulted in "bursts of locomotor activity lasting between 3 and 5 minutes, after which they remained immobile but alert," but with no more than minimal signs of seizure. With regard to c-fos expression, rats treated with RF + picrotoxin exhibited 2-4 times the number of positive staining neurons in limbic structures, olfactory cortex areas and subcortical areas, the dentate gyrus, and the central lateral nucleus of the thalamic intralaminar nucleus group than rats treated with picrotoxin alone. In rats not treated with picrotoxin, c-Fos counts were low and were not affected by RF-exposure. The authors suggest that because of the low SAR, the effects were not likely to be a result of temperature increases and suggest that in seizure-prone rats (and epileptic humans) the sensitivity to RF exposure from mobile phones may be different. AUTHORS' ABSTRACT: Jorge-Mora et al. 2011 (#5101): This study investigated the effects of microwave radiation on the PVN of the hypothalamus, extracted from rat brains. Expression of c-Fos was used to study the pattern of cellular activation in rats exposed once or repeatedly (ten times in 2 weeks) to 2.45 GHz radiation in a GTEM cell. The power intensities used were 3 and 12 W and the Finite Difference Time Domain calculation was used to determine the specific absorption rate (SAR). High SAR triggered an increase of the c-Fos marker 90 min or 24 h after radiation, and low SAR resulted in c-Fos counts higher than in control rats after 24 h. Repeated irradiation at 3 W increased cellular activation of PVN by more than 100% compared to animals subjected to acute irradiation and to repeated non-radiated repeated session control animals. The results suggest that PVN is sensitive to 2.45 GHz microwave radiation at non-thermal SAR levels. AUTHORS' ABSTRACT: Carballo-Quintas et al. 2011 (IEEE #6257): The acute effects of microwave exposure from the Global System for Mobile Communication (GSM) were studied in rats, using 900MHz radiation at an intensity similar to mobile phone emissions. Acute subconvulsive doses of picrotoxin were then administered to the rats and an experimental model of seizure-proneness was created from the data. Seventy-two adult male Sprague-Dawley rats underwent immunochemical testing of relevant anatomical areas to measure induction of the c-fos neuronal marker after 90min and 24h, and of the glial fibrillary acidic protein (GFAP) 72h after acute exposure to a 900MHz electromagnetic field (EMF). The experimental set-up facilitated measurement of absorbed power, from which the average specific absorption rate was calculated using the finite-difference time-domain (FDTD) 2h after exposure to EMF radiation at 1.45W/kg in picrotoxin-treated rats and 1.38W/kg in untreated rats. Ninety minutes after radiation high levels of c-fos expression were recorded in the neocortex and paleocortex along with low hippocampus activation in picrotoxin treated animals. Most brain areas, except the limbic cortical region, showed important increases in neuronal activation 24h after picrotoxin and radiation. Three days after picrotoxin treatment, radiation effects were still apparent in the neocortex, dentate gyrus and CA3, but a significant decrease in activity was noted in the piriform and entorhinal cortex. During this time, glial reactivity increased with every seizure in irradiated, picrotoxin-treated brain regions. Our results reveal that c-fos and glial markers were triggered by the combined stress of non-thermal irradiation and the toxic effect of picrotoxin on cerebral tissues. AUTHORS' ABSTRACT: Jorge-Mora et al. 2010 (IEEE #6261): Physical agents such as non-ionizing continuous-wave 2.45 GHz radiation may cause damage that alters cellular homeostasis and may trigger activation of the genes that encode heat shock proteins (HSP). We used Enzyme-Linked ImmunoSorbent Assay (ELI-SA) and immunohistochemistry to analyze the changes in levels of HSP-90 and its distribution in the brain of Sprague-Dawley rats, ninety minutes and twenty-four hours after acute (30 min) continuous exposure to 2.45 GHz radiation in a the Gigahertz Transverse Electromagnetic (GTEM cell). In addition, we studied further indicators of neuronal insult: dark neurons, chromatin condensation and nucleus fragmentation, which were observed under optical conventional or fluorescence microscopy after DAPI staining. The cellular distribution of protein HSP-90 in the brain increased with each corresponding (0.034 ± 3.10-3, 0.069 ± 5.10-3, 0.27 ± 21.10-3 W/kg), in hypothalamic nuclei, limbic cortex and somatosensorial cortex after exposure to the radiation. At twenty-four hours post-irradiation, levels of HSP-90 protein remained high in all hypothalamic nuclei for all SARs, and in the parietal cortex, except the limbic system, HSP-90 levels were lower than in non-irradiated rats, almost half the levels in rats exposed to the highest power radiation. Non-apoptotic cellular nuclei and a some dark neurons were found ninety minutes and twenty-four hours after maximal SAR exposure. The results suggest that acute exposure to electromagnetic fields triggered an imbalance in anatomical HSP-90 levels but the anti-apoptotic mechanism is probably sufficient to compensate the non-ionizing stimulus. Further studies are required to determine the regional effects of chronic electromagnetic pollution on heat shock proteins and their involvement in neurological processes and neuronal damage. AUTHORS' ABSTRACT: Misa-Agustino et al. 2012 (IEEE #6282): Non-ionizing radiation at 2.45 GHz may modify the expression of genes that codify heat shock proteins (HSP) in the thyroid gland. Using the enzyme-linked immunosorbent assay (ELISA) technique, we studied levels of HSP-90 and HSP-70. We also used hematoxilin eosin to look for evidence of lesions in the gland and applied the DAPI technique of fluorescence to search for evidence of chromatin condensation and nuclear fragmentation in the thyroid cells of adult female Sprague-Dawley rats. Fiftyfour rats were individually exposed for 30 min to 2.45 GHz radiation in a Gigahertz transverse electromagnetic (GTEM) cell at different levels of non-thermal specific absorption rate (SAR), which was calculated using the finite difference time domain (FDTD) technique. Ninetyminutes after radiation,HSP-90 and HSP-70 had decreased significantly (P,0.01) after applying a SAR of 0.04661.10 W/Kg or 0.10465.1023 W/Kg. Twenty-four hours after radiation, HSP-90 had partially recovered and HSP-70 had recovered completely. There were few indications of lesions in the glandular structure and signs of apoptosis were negative in all radiated animals. The results suggest that acute sub-thermal radiation at 2.45 GHz may alter levels of cellular stress in rat thyroid gland without initially altering their anti-apoptotic capacity. AUTHORS' ABSTRACT: Misa-Agustino et al. 2015 (IEEE #6283): AIMS: Electromagnetic fields (EMFs) can act as inducers or mediators of stress response through the production of heat shock proteins (HSPs) that modulate immune response and thymus functions. In this study, we analyzed cellular stress levels in rat thymus after exposure of the rats to a 2.45 GHz radio frequency (RF) using an experimental diathermic model in a Gigahertz Transverse Electromagnetic (GTEM) chamber. MAIN METHODS: In this experiment, we used H&E staining, the ELISA test and immunohistochemistry to examine Hsp70 and Hsp90 expression in the thymus and glucocorticoid receptors (GR) of 64 female SpragueDawley rats exposed individually to 2.45 GHz (at 0, 1.5, 3.0 or 12.0 W power). The 1 g averaged peak and mean SAR values in the thymus and whole body of each rat to ensure that sub-thermal levels of radiation were being reached. KEY FINDINGS: The thymus tissue presented several morphological changes, including increased distribution of blood vessels along with the appearance of red blood cells and hemorrhagic reticuloepithelial cells. Levels of Hsp90 decreased in the thymus when animals were exposed to the highest power level (12 W), but only one group did not show recovery after 24 h. Hsp70 presented no significant modifications in any of the groups. The glucocorticoid receptors presented greater immunomarking on the thymic cortex in exposed animals. SIGNIFICANCE: Our results indicate that non-ionizing sub-thermal radiation causes changes in the endothelial permeability and vascularization of the thymus, and is a tissue-modulating agent for Hsp90 and GR. AUTHORS' ABSTRACT: Furelos et al. 2016 (IEEE #6483): Multiple simultaneous exposures to electromagnetic signals induced adjustments in mammal nervous systems. In this study, we investigated the non-thermal SAR (Specific Absorption Rate) in the cerebral or cerebellar hemispheres of rats exposed in vivo to combined electromagnetic field (EMF) signals at 900 and 2450 MHz.Forty rats divided into four groups of 10 were individually exposed or not exposed to radiation in a GTEM chamber for one or two hours. After radiation, we used the Chemiluminescent Enzyme-Linked Immunosorbent Assay (ChELISA) technique to measure cellular stress levels, indicated by the presence of heat shock proteins (HSP) 90 and 70, as well as caspase-3-dependent pre-apoptotic activity in left and right cerebral and cerebellar hemispheres of Sprague Dawley rats.Twenty-four hours after exposure to combined or single radiation, significant differences were evident in HSP 90 and 70 but not in caspase 3 levels between the hemispheres of the cerebral cortex at high SAR levels. In the cerebellar hemispheres, groups exposed to a single radiofrequency (RF) and high SAR showed significant differences in HSP 90, 70 and caspase-3 levels compared to control animals. The absorbed energy and/or biological effects of combined signals were not additive, suggesting that multiple signals act on nervous tissue by a different mechanism. AUTHORS'ABSTRACT: Relova et al. 2010 (IEEE #6968) (NOT PEER REVIEWED): Considerable concern has been expressed about the possible health risks of mobile-phone use. The brain has greater exposure to mObile-phone radiation (MPR) than the rest of the body, and there are experimental findings suggesting that electromagnetic fields may modulate the activity of neural networks. The tendency towards electrical instability of the neural networks of epileptics suggests that these persons may be especially sensitive to electromagnetic radiation. In this study, we determined the effects ormobile-phone radiation on the electroencephalographic (EEGy speCtra of nine epileptic patients undergoing routine video-EEG monitoring. For each of nine scalp areas and four wavebands (alpha, beta, gamma, and delta), three spectral features were extracted from EEG segments recorded before, during, and after 20 minutes of continuous exposure to mobile-phone radiation. Statistical analyses showed associÀ1tions between mobile-phonÀ2 rÀ3diation and increased EEG activity in the alpha, beta, and gamma wavebands. The increase In alpha-wave power was similar to that reported for non-epileptic individuals. The increase in beta- and gamma-wave power may be related to epileptic alterations. |
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| Findings | Effects | |
| Status | Completed With Publication | |
| Principal Investigator | University of Santiago de Compostela, Spain | |
| Funding Agency | Nat'l Res Prog, Spain | |
| Country | SPAIN | |
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