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Gamma radiation at a human relevant low dose rate is genotoxic in mice
Even today, 70 years after Hiroshima and accidents like in Chernobyl and Fukushima, we still have limited knowledge about the health effects of low dose rate (LDR) radiation. Despite their human relevance after occupational and accidental exposure, only few animal studies on the genotoxic effects of...
Autores principales: | , , , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group
2016
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5011728/ https://www.ncbi.nlm.nih.gov/pubmed/27596356 http://dx.doi.org/10.1038/srep32977 |
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author | Graupner, Anne Eide, Dag M. Instanes, Christine Andersen, Jill M. Brede, Dag A. Dertinger, Stephen D. Lind, Ole C. Brandt-Kjelsen, Anicke Bjerke, Hans Salbu, Brit Oughton, Deborah Brunborg, Gunnar Olsen, Ann K. |
author_facet | Graupner, Anne Eide, Dag M. Instanes, Christine Andersen, Jill M. Brede, Dag A. Dertinger, Stephen D. Lind, Ole C. Brandt-Kjelsen, Anicke Bjerke, Hans Salbu, Brit Oughton, Deborah Brunborg, Gunnar Olsen, Ann K. |
author_sort | Graupner, Anne |
collection | PubMed |
description | Even today, 70 years after Hiroshima and accidents like in Chernobyl and Fukushima, we still have limited knowledge about the health effects of low dose rate (LDR) radiation. Despite their human relevance after occupational and accidental exposure, only few animal studies on the genotoxic effects of chronic LDR radiation have been performed. Selenium (Se) is involved in oxidative stress defence, protecting DNA and other biomolecules from reactive oxygen species (ROS). It is hypothesised that Se deficiency, as it occurs in several parts of the world, may aggravate harmful effects of ROS-inducing stressors such as ionising radiation. We performed a study in the newly established LDR-facility Figaro on the combined effects of Se deprivation and LDR γ exposure in DNA repair knockout mice (Ogg1(−/−)) and control animals (Ogg1(+/−)). Genotoxic effects were seen after continuous radiation (1.4 mGy/h) for 45 days. Chromosomal damage (micronucleus), phenotypic mutations (Pig-a gene mutation of RBC(CD24−)) and DNA lesions (single strand breaks/alkali labile sites) were significantly increased in blood cells of irradiated animals, covering three types of genotoxic activity. This study demonstrates that chronic LDR γ radiation is genotoxic in an exposure scenario realistic for humans, supporting the hypothesis that even LDR γ radiation may induce cancer. |
format | Online Article Text |
id | pubmed-5011728 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2016 |
publisher | Nature Publishing Group |
record_format | MEDLINE/PubMed |
spelling | pubmed-50117282016-09-12 Gamma radiation at a human relevant low dose rate is genotoxic in mice Graupner, Anne Eide, Dag M. Instanes, Christine Andersen, Jill M. Brede, Dag A. Dertinger, Stephen D. Lind, Ole C. Brandt-Kjelsen, Anicke Bjerke, Hans Salbu, Brit Oughton, Deborah Brunborg, Gunnar Olsen, Ann K. Sci Rep Article Even today, 70 years after Hiroshima and accidents like in Chernobyl and Fukushima, we still have limited knowledge about the health effects of low dose rate (LDR) radiation. Despite their human relevance after occupational and accidental exposure, only few animal studies on the genotoxic effects of chronic LDR radiation have been performed. Selenium (Se) is involved in oxidative stress defence, protecting DNA and other biomolecules from reactive oxygen species (ROS). It is hypothesised that Se deficiency, as it occurs in several parts of the world, may aggravate harmful effects of ROS-inducing stressors such as ionising radiation. We performed a study in the newly established LDR-facility Figaro on the combined effects of Se deprivation and LDR γ exposure in DNA repair knockout mice (Ogg1(−/−)) and control animals (Ogg1(+/−)). Genotoxic effects were seen after continuous radiation (1.4 mGy/h) for 45 days. Chromosomal damage (micronucleus), phenotypic mutations (Pig-a gene mutation of RBC(CD24−)) and DNA lesions (single strand breaks/alkali labile sites) were significantly increased in blood cells of irradiated animals, covering three types of genotoxic activity. This study demonstrates that chronic LDR γ radiation is genotoxic in an exposure scenario realistic for humans, supporting the hypothesis that even LDR γ radiation may induce cancer. Nature Publishing Group 2016-09-06 /pmc/articles/PMC5011728/ /pubmed/27596356 http://dx.doi.org/10.1038/srep32977 Text en Copyright © 2016, The Author(s) http://creativecommons.org/licenses/by/4.0/ This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/ |
spellingShingle | Article Graupner, Anne Eide, Dag M. Instanes, Christine Andersen, Jill M. Brede, Dag A. Dertinger, Stephen D. Lind, Ole C. Brandt-Kjelsen, Anicke Bjerke, Hans Salbu, Brit Oughton, Deborah Brunborg, Gunnar Olsen, Ann K. Gamma radiation at a human relevant low dose rate is genotoxic in mice |
title | Gamma radiation at a human relevant low dose rate is genotoxic in mice |
title_full | Gamma radiation at a human relevant low dose rate is genotoxic in mice |
title_fullStr | Gamma radiation at a human relevant low dose rate is genotoxic in mice |
title_full_unstemmed | Gamma radiation at a human relevant low dose rate is genotoxic in mice |
title_short | Gamma radiation at a human relevant low dose rate is genotoxic in mice |
title_sort | gamma radiation at a human relevant low dose rate is genotoxic in mice |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5011728/ https://www.ncbi.nlm.nih.gov/pubmed/27596356 http://dx.doi.org/10.1038/srep32977 |
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