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Aging and radiation: bad companions

Aging involves a deterioration of cell functions and changes that may predispose the cell to undergo an oncogenic transformation. The carcinogenic risks following radiation exposure rise with age among adults. Increasing inflammatory response, loss of oxidant/antioxidant equilibrium, ongoing telomer...

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Autores principales: Hernández, Laia, Terradas, Mariona, Camps, Jordi, Martín, Marta, Tusell, Laura, Genescà, Anna
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BlackWell Publishing Ltd 2015
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4364827/
https://www.ncbi.nlm.nih.gov/pubmed/25645467
http://dx.doi.org/10.1111/acel.12306
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author Hernández, Laia
Terradas, Mariona
Camps, Jordi
Martín, Marta
Tusell, Laura
Genescà, Anna
author_facet Hernández, Laia
Terradas, Mariona
Camps, Jordi
Martín, Marta
Tusell, Laura
Genescà, Anna
author_sort Hernández, Laia
collection PubMed
description Aging involves a deterioration of cell functions and changes that may predispose the cell to undergo an oncogenic transformation. The carcinogenic risks following radiation exposure rise with age among adults. Increasing inflammatory response, loss of oxidant/antioxidant equilibrium, ongoing telomere attrition, decline in the DNA damage response efficiency, and deleterious nuclear organization are age-related cellular changes that trigger a serious threat to genomic integrity. In this review, we discuss the mechanistic interplay between all these factors, providing an integrated view of how they contribute to the observed age-related increase in radiation sensitivity. As life expectancy increases and so it does the medical intervention, it is important to highlight the benefits of radiation protection in the elderly. Thus, a deep understanding of the mechanistic processes confining the threat of aging-related radiosensitivity is currently of foremost relevance.
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spelling pubmed-43648272015-04-01 Aging and radiation: bad companions Hernández, Laia Terradas, Mariona Camps, Jordi Martín, Marta Tusell, Laura Genescà, Anna Aging Cell Review Aging involves a deterioration of cell functions and changes that may predispose the cell to undergo an oncogenic transformation. The carcinogenic risks following radiation exposure rise with age among adults. Increasing inflammatory response, loss of oxidant/antioxidant equilibrium, ongoing telomere attrition, decline in the DNA damage response efficiency, and deleterious nuclear organization are age-related cellular changes that trigger a serious threat to genomic integrity. In this review, we discuss the mechanistic interplay between all these factors, providing an integrated view of how they contribute to the observed age-related increase in radiation sensitivity. As life expectancy increases and so it does the medical intervention, it is important to highlight the benefits of radiation protection in the elderly. Thus, a deep understanding of the mechanistic processes confining the threat of aging-related radiosensitivity is currently of foremost relevance. BlackWell Publishing Ltd 2015-04 2015-02-02 /pmc/articles/PMC4364827/ /pubmed/25645467 http://dx.doi.org/10.1111/acel.12306 Text en © 2015 The Authors. Aging Cell published by the Anatomical Society and John Wiley & Sons Ltd. http://creativecommons.org/licenses/by/4.0/ This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
spellingShingle Review
Hernández, Laia
Terradas, Mariona
Camps, Jordi
Martín, Marta
Tusell, Laura
Genescà, Anna
Aging and radiation: bad companions
title Aging and radiation: bad companions
title_full Aging and radiation: bad companions
title_fullStr Aging and radiation: bad companions
title_full_unstemmed Aging and radiation: bad companions
title_short Aging and radiation: bad companions
title_sort aging and radiation: bad companions
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4364827/
https://www.ncbi.nlm.nih.gov/pubmed/25645467
http://dx.doi.org/10.1111/acel.12306
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