Jorge-Mora T., M. Alvarez-Folgueiras, J. Leiro, F.

EXPOSURE TO 2.45 GHz MICROWAVE RADIATION PROVOKES CEREBRAL CHANGES IN INDUCTION OF HSP-90 α HEAT SHOCK PROTEIN IN RAT
Progress In Electromagnetics Research, PIER 100, 351-379, 2010

T. Jorge-Mora, M. Alvarez-Folgueiras, J. Leiro, F. J. Jorge-Barreiro, F. J. Ares-Pena, E. Lopez-Martin
Morphological Sciences Department, University of Santiago de Compostela, 15782 Santiago de Compostela, Spain
Applied Physics Department, University of Santiago de Compostela, 15782 Santiago de Compostela, Spain
Institute of Food Research and Analysis, University of Santiago de Compostela,
15782 Santiago de Compostela, Spain

2450 MHz CW
0,034; 0,069; 0,27 SAR

Abstract
- 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 (ELISA) 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 (30min) continuous exposure to 2.45 GHz radiation in a 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 SAR (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 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.

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