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Role of Oxidative RNA Damage in Chronic-Degenerative Diseases

Normal cellular metabolism and exposure to ionizing and ultraviolet radiations and exogenous agents produce reactive oxygen species (ROS). Due to their reactivity, they can interact with many critical biomolecules and induce cell damage. The reaction of ROS with free nucleobases, nucleosides, nucleo...

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Detalles Bibliográficos
Autor principal: Fimognari, Carmela
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi Publishing Corporation 2015
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4452857/
https://www.ncbi.nlm.nih.gov/pubmed/26078805
http://dx.doi.org/10.1155/2015/358713
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author Fimognari, Carmela
author_facet Fimognari, Carmela
author_sort Fimognari, Carmela
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description Normal cellular metabolism and exposure to ionizing and ultraviolet radiations and exogenous agents produce reactive oxygen species (ROS). Due to their reactivity, they can interact with many critical biomolecules and induce cell damage. The reaction of ROS with free nucleobases, nucleosides, nucleotides, or oligonucleotides can generate numerous distinct modifications in nucleic acids. Oxidative damage to DNA has been widely investigated and is strongly implicated in the development of many chronic-degenerative diseases. In contrast, RNA damage is a poorly examined field in biomedical research. In this review, I discuss the importance of RNA as a target of oxidative damage and the role of oxidative damage to RNA in the pathogenesis of some chronic-degenerative diseases, such as neurological disorders, atherosclerosis, and cancer. Furthermore, I review recent evidence suggesting that RNA may be the target for toxic agents and indicating RNA degradation as a powerful tool to treat any pathology in which there is an aberrant expression of mRNA and/or its gene products.
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spelling pubmed-44528572015-06-15 Role of Oxidative RNA Damage in Chronic-Degenerative Diseases Fimognari, Carmela Oxid Med Cell Longev Review Article Normal cellular metabolism and exposure to ionizing and ultraviolet radiations and exogenous agents produce reactive oxygen species (ROS). Due to their reactivity, they can interact with many critical biomolecules and induce cell damage. The reaction of ROS with free nucleobases, nucleosides, nucleotides, or oligonucleotides can generate numerous distinct modifications in nucleic acids. Oxidative damage to DNA has been widely investigated and is strongly implicated in the development of many chronic-degenerative diseases. In contrast, RNA damage is a poorly examined field in biomedical research. In this review, I discuss the importance of RNA as a target of oxidative damage and the role of oxidative damage to RNA in the pathogenesis of some chronic-degenerative diseases, such as neurological disorders, atherosclerosis, and cancer. Furthermore, I review recent evidence suggesting that RNA may be the target for toxic agents and indicating RNA degradation as a powerful tool to treat any pathology in which there is an aberrant expression of mRNA and/or its gene products. Hindawi Publishing Corporation 2015 2015-05-20 /pmc/articles/PMC4452857/ /pubmed/26078805 http://dx.doi.org/10.1155/2015/358713 Text en Copyright © 2015 Carmela Fimognari. https://creativecommons.org/licenses/by/3.0/ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Review Article
Fimognari, Carmela
Role of Oxidative RNA Damage in Chronic-Degenerative Diseases
title Role of Oxidative RNA Damage in Chronic-Degenerative Diseases
title_full Role of Oxidative RNA Damage in Chronic-Degenerative Diseases
title_fullStr Role of Oxidative RNA Damage in Chronic-Degenerative Diseases
title_full_unstemmed Role of Oxidative RNA Damage in Chronic-Degenerative Diseases
title_short Role of Oxidative RNA Damage in Chronic-Degenerative Diseases
title_sort role of oxidative rna damage in chronic-degenerative diseases
topic Review Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4452857/
https://www.ncbi.nlm.nih.gov/pubmed/26078805
http://dx.doi.org/10.1155/2015/358713
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