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Oxidative Stress Associated with Neuronal Apoptosis in Experimental Models of Epilepsy
Epilepsy is considered one of the most common neurological disorders worldwide. Oxidative stress produced by free radicals may play a role in the initiation and progression of epilepsy; the changes in the mitochondrial and the oxidative stress state can lead mechanism associated with neuronal death...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Hindawi Publishing Corporation
2014
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4295154/ https://www.ncbi.nlm.nih.gov/pubmed/25614776 http://dx.doi.org/10.1155/2014/293689 |
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author | Méndez-Armenta, Marisela Nava-Ruíz, Concepción Juárez-Rebollar, Daniel Rodríguez-Martínez, Erika Yescas Gómez, Petra |
author_facet | Méndez-Armenta, Marisela Nava-Ruíz, Concepción Juárez-Rebollar, Daniel Rodríguez-Martínez, Erika Yescas Gómez, Petra |
author_sort | Méndez-Armenta, Marisela |
collection | PubMed |
description | Epilepsy is considered one of the most common neurological disorders worldwide. Oxidative stress produced by free radicals may play a role in the initiation and progression of epilepsy; the changes in the mitochondrial and the oxidative stress state can lead mechanism associated with neuronal death pathway. Bioenergetics state failure and impaired mitochondrial function include excessive free radical production with impaired synthesis of antioxidants. This review summarizes evidence that suggest what is the role of oxidative stress on induction of apoptosis in experimental models of epilepsy. |
format | Online Article Text |
id | pubmed-4295154 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2014 |
publisher | Hindawi Publishing Corporation |
record_format | MEDLINE/PubMed |
spelling | pubmed-42951542015-01-22 Oxidative Stress Associated with Neuronal Apoptosis in Experimental Models of Epilepsy Méndez-Armenta, Marisela Nava-Ruíz, Concepción Juárez-Rebollar, Daniel Rodríguez-Martínez, Erika Yescas Gómez, Petra Oxid Med Cell Longev Review Article Epilepsy is considered one of the most common neurological disorders worldwide. Oxidative stress produced by free radicals may play a role in the initiation and progression of epilepsy; the changes in the mitochondrial and the oxidative stress state can lead mechanism associated with neuronal death pathway. Bioenergetics state failure and impaired mitochondrial function include excessive free radical production with impaired synthesis of antioxidants. This review summarizes evidence that suggest what is the role of oxidative stress on induction of apoptosis in experimental models of epilepsy. Hindawi Publishing Corporation 2014 2014-12-29 /pmc/articles/PMC4295154/ /pubmed/25614776 http://dx.doi.org/10.1155/2014/293689 Text en Copyright © 2014 Marisela Méndez-Armenta et al. 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 Méndez-Armenta, Marisela Nava-Ruíz, Concepción Juárez-Rebollar, Daniel Rodríguez-Martínez, Erika Yescas Gómez, Petra Oxidative Stress Associated with Neuronal Apoptosis in Experimental Models of Epilepsy |
title | Oxidative Stress Associated with Neuronal Apoptosis in Experimental Models of Epilepsy |
title_full | Oxidative Stress Associated with Neuronal Apoptosis in Experimental Models of Epilepsy |
title_fullStr | Oxidative Stress Associated with Neuronal Apoptosis in Experimental Models of Epilepsy |
title_full_unstemmed | Oxidative Stress Associated with Neuronal Apoptosis in Experimental Models of Epilepsy |
title_short | Oxidative Stress Associated with Neuronal Apoptosis in Experimental Models of Epilepsy |
title_sort | oxidative stress associated with neuronal apoptosis in experimental models of epilepsy |
topic | Review Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4295154/ https://www.ncbi.nlm.nih.gov/pubmed/25614776 http://dx.doi.org/10.1155/2014/293689 |
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