Electromagnetic fields at 2.45 GHz trigger changes in heat shock proteins 90 and 70 without altering apoptotic activity in rat thyroid gland

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 t...

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Main Authors: Misa Agustiño, María José, Leiro, José Manuel, Jorge Mora, María Teresa, Rodríguez-González, Juan Antonio, Jorge Barreiro, Francisco Javier, Ares-Pena, Francisco José, López-Martín, Elena
Format: Online
Language:English
Published: The Company of Biologists 2012
Online Access:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3507243/
id pubmed-3507243
recordtype oai_dc
spelling pubmed-35072432012-12-04 Electromagnetic fields at 2.45 GHz trigger changes in heat shock proteins 90 and 70 without altering apoptotic activity in rat thyroid gland Misa Agustiño, María José Leiro, José Manuel Jorge Mora, María Teresa Rodríguez-González, Juan Antonio Jorge Barreiro, Francisco Javier Ares-Pena, Francisco José López-Martín, Elena Research Article 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. Fifty-four 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. Ninety minutes after radiation, HSP-90 and HSP-70 had decreased significantly (P<0.01) after applying a SAR of 0.046±1.10 W/Kg or 0.104±5.10−3 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. The Company of Biologists 2012-07-09 /pmc/articles/PMC3507243/ /pubmed/23213477 http://dx.doi.org/10.1242/bio.20121297 Text en © 2012. Published by The Company of Biologists Ltd http://creativecommons.org/licenses/by-nc-sa/3.0 This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial Share Alike License (http://creativecommons.org/licenses/by-nc-sa/3.0/).
repository_type Open Access Journal
institution_category Foreign Institution
institution US National Center for Biotechnology Information
building NCBI PubMed
collection Online Access
language English
format Online
author Misa Agustiño, María José
Leiro, José Manuel
Jorge Mora, María Teresa
Rodríguez-González, Juan Antonio
Jorge Barreiro, Francisco Javier
Ares-Pena, Francisco José
López-Martín, Elena
spellingShingle Misa Agustiño, María José
Leiro, José Manuel
Jorge Mora, María Teresa
Rodríguez-González, Juan Antonio
Jorge Barreiro, Francisco Javier
Ares-Pena, Francisco José
López-Martín, Elena
Electromagnetic fields at 2.45 GHz trigger changes in heat shock proteins 90 and 70 without altering apoptotic activity in rat thyroid gland
author_facet Misa Agustiño, María José
Leiro, José Manuel
Jorge Mora, María Teresa
Rodríguez-González, Juan Antonio
Jorge Barreiro, Francisco Javier
Ares-Pena, Francisco José
López-Martín, Elena
author_sort Misa Agustiño, María José
title Electromagnetic fields at 2.45 GHz trigger changes in heat shock proteins 90 and 70 without altering apoptotic activity in rat thyroid gland
title_short Electromagnetic fields at 2.45 GHz trigger changes in heat shock proteins 90 and 70 without altering apoptotic activity in rat thyroid gland
title_full Electromagnetic fields at 2.45 GHz trigger changes in heat shock proteins 90 and 70 without altering apoptotic activity in rat thyroid gland
title_fullStr Electromagnetic fields at 2.45 GHz trigger changes in heat shock proteins 90 and 70 without altering apoptotic activity in rat thyroid gland
title_full_unstemmed Electromagnetic fields at 2.45 GHz trigger changes in heat shock proteins 90 and 70 without altering apoptotic activity in rat thyroid gland
title_sort electromagnetic fields at 2.45 ghz trigger changes in heat shock proteins 90 and 70 without altering apoptotic activity in rat thyroid gland
description 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. Fifty-four 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. Ninety minutes after radiation, HSP-90 and HSP-70 had decreased significantly (P<0.01) after applying a SAR of 0.046±1.10 W/Kg or 0.104±5.10−3 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.
publisher The Company of Biologists
publishDate 2012
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3507243/
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