Ionizing Radiation and Human Health: Reviewing Models of Exposure and Mechanisms of Cellular Damage. An Epigenetic Perspective
We reviewed available evidence in medical literature concerning experimental models of exposure to ionizing radiations (IR) and their mechanisms of producing damages on living organisms. The traditional model is based on the theory of “stochastic breakage” of one or both strands...
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doaj-5559693eaa8245f4a5f6b540d810a1d12020-11-25T00:42:04ZengMDPI AGInternational Journal of Environmental Research and Public Health1660-46012018-09-01159197110.3390/ijerph15091971ijerph15091971Ionizing Radiation and Human Health: Reviewing Models of Exposure and Mechanisms of Cellular Damage. An Epigenetic PerspectiveErnesto Burgio0Prisco Piscitelli1Lucia Migliore2European Cancer and Environment Research-ECERI, 1000 Bruxelles, BelgiumEuro Mediterranean Scientific Biomedical Institute-ISBEM Research Centre, 72023 Mesagne (Brindisi), ItalyDepartment of Translational Research and New Technologies in Medicine and Surgery, University of Pisa, 56126 Pisa, ItalyWe reviewed available evidence in medical literature concerning experimental models of exposure to ionizing radiations (IR) and their mechanisms of producing damages on living organisms. The traditional model is based on the theory of “stochastic breakage” of one or both strands of the DNA double helix. According to this model, high doses may cause the breaks, potentially lethal to the cell by damaging both DNA strands, while low doses of IR would cause essentially single strands breaks, easily repairable, resulting in no permanent damages. The available evidence makes this classical model increasingly less acceptable, because the exposure to low doses of IR seems to have carcinogenic effects, even after years or decades, both in the exposed individuals and in subsequent generations. In addition, the cells that survived the exposure to low doses, despite being apparently normal, accumulate damages that become evident in their progeny, such as nonclonal chromosomal aberrations, which can be found even in cells not directly irradiated due to the exchange of molecular signals and complex tissue reactions involving neighboring or distant cells. For all these reasons, a paradigm shift is needed, based on evidence and epigenetics.http://www.mdpi.com/1660-4601/15/9/1971ionizing radiationscellular damagecarcinogenic mechanismsepigenetic mechanisms |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Ernesto Burgio Prisco Piscitelli Lucia Migliore |
spellingShingle |
Ernesto Burgio Prisco Piscitelli Lucia Migliore Ionizing Radiation and Human Health: Reviewing Models of Exposure and Mechanisms of Cellular Damage. An Epigenetic Perspective International Journal of Environmental Research and Public Health ionizing radiations cellular damage carcinogenic mechanisms epigenetic mechanisms |
author_facet |
Ernesto Burgio Prisco Piscitelli Lucia Migliore |
author_sort |
Ernesto Burgio |
title |
Ionizing Radiation and Human Health: Reviewing Models of Exposure and Mechanisms of Cellular Damage. An Epigenetic Perspective |
title_short |
Ionizing Radiation and Human Health: Reviewing Models of Exposure and Mechanisms of Cellular Damage. An Epigenetic Perspective |
title_full |
Ionizing Radiation and Human Health: Reviewing Models of Exposure and Mechanisms of Cellular Damage. An Epigenetic Perspective |
title_fullStr |
Ionizing Radiation and Human Health: Reviewing Models of Exposure and Mechanisms of Cellular Damage. An Epigenetic Perspective |
title_full_unstemmed |
Ionizing Radiation and Human Health: Reviewing Models of Exposure and Mechanisms of Cellular Damage. An Epigenetic Perspective |
title_sort |
ionizing radiation and human health: reviewing models of exposure and mechanisms of cellular damage. an epigenetic perspective |
publisher |
MDPI AG |
series |
International Journal of Environmental Research and Public Health |
issn |
1660-4601 |
publishDate |
2018-09-01 |
description |
We reviewed available evidence in medical literature concerning experimental models of exposure to ionizing radiations (IR) and their mechanisms of producing damages on living organisms. The traditional model is based on the theory of “stochastic breakage” of one or both strands of the DNA double helix. According to this model, high doses may cause the breaks, potentially lethal to the cell by damaging both DNA strands, while low doses of IR would cause essentially single strands breaks, easily repairable, resulting in no permanent damages. The available evidence makes this classical model increasingly less acceptable, because the exposure to low doses of IR seems to have carcinogenic effects, even after years or decades, both in the exposed individuals and in subsequent generations. In addition, the cells that survived the exposure to low doses, despite being apparently normal, accumulate damages that become evident in their progeny, such as nonclonal chromosomal aberrations, which can be found even in cells not directly irradiated due to the exchange of molecular signals and complex tissue reactions involving neighboring or distant cells. For all these reasons, a paradigm shift is needed, based on evidence and epigenetics. |
topic |
ionizing radiations cellular damage carcinogenic mechanisms epigenetic mechanisms |
url |
http://www.mdpi.com/1660-4601/15/9/1971 |
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