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Lipids and Oxidative Stress Associated with Ethanol-Induced Neurological Damage

The excessive intake of alcohol is a serious public health problem, especially given the severe damage provoked by chronic or prenatal exposure to alcohol that affects many physiological processes, such as memory, motor function, and cognitive abilities. This damage is related to the ethanol oxidati...

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Autores principales: Hernández, José A., López-Sánchez, Rosa C., Rendón-Ramírez, Adela
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi Publishing Corporation 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4753689/
https://www.ncbi.nlm.nih.gov/pubmed/26949445
http://dx.doi.org/10.1155/2016/1543809
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author Hernández, José A.
López-Sánchez, Rosa C.
Rendón-Ramírez, Adela
author_facet Hernández, José A.
López-Sánchez, Rosa C.
Rendón-Ramírez, Adela
author_sort Hernández, José A.
collection PubMed
description The excessive intake of alcohol is a serious public health problem, especially given the severe damage provoked by chronic or prenatal exposure to alcohol that affects many physiological processes, such as memory, motor function, and cognitive abilities. This damage is related to the ethanol oxidation in the brain. The metabolism of ethanol to acetaldehyde and then to acetate is associated with the production of reactive oxygen species that accentuate the oxidative state of cells. This metabolism of ethanol can induce the oxidation of the fatty acids in phospholipids, and the bioactive aldehydes produced are known to be associated with neurotoxicity and neurodegeneration. As such, here we will review the role of lipids in the neuronal damage induced by ethanol-related oxidative stress and the role that lipids play in the related compensatory or defense mechanisms.
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spelling pubmed-47536892016-03-06 Lipids and Oxidative Stress Associated with Ethanol-Induced Neurological Damage Hernández, José A. López-Sánchez, Rosa C. Rendón-Ramírez, Adela Oxid Med Cell Longev Review Article The excessive intake of alcohol is a serious public health problem, especially given the severe damage provoked by chronic or prenatal exposure to alcohol that affects many physiological processes, such as memory, motor function, and cognitive abilities. This damage is related to the ethanol oxidation in the brain. The metabolism of ethanol to acetaldehyde and then to acetate is associated with the production of reactive oxygen species that accentuate the oxidative state of cells. This metabolism of ethanol can induce the oxidation of the fatty acids in phospholipids, and the bioactive aldehydes produced are known to be associated with neurotoxicity and neurodegeneration. As such, here we will review the role of lipids in the neuronal damage induced by ethanol-related oxidative stress and the role that lipids play in the related compensatory or defense mechanisms. Hindawi Publishing Corporation 2016 2016-01-05 /pmc/articles/PMC4753689/ /pubmed/26949445 http://dx.doi.org/10.1155/2016/1543809 Text en Copyright © 2016 José A. Hernández et al. https://creativecommons.org/licenses/by/4.0/ 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
Hernández, José A.
López-Sánchez, Rosa C.
Rendón-Ramírez, Adela
Lipids and Oxidative Stress Associated with Ethanol-Induced Neurological Damage
title Lipids and Oxidative Stress Associated with Ethanol-Induced Neurological Damage
title_full Lipids and Oxidative Stress Associated with Ethanol-Induced Neurological Damage
title_fullStr Lipids and Oxidative Stress Associated with Ethanol-Induced Neurological Damage
title_full_unstemmed Lipids and Oxidative Stress Associated with Ethanol-Induced Neurological Damage
title_short Lipids and Oxidative Stress Associated with Ethanol-Induced Neurological Damage
title_sort lipids and oxidative stress associated with ethanol-induced neurological damage
topic Review Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4753689/
https://www.ncbi.nlm.nih.gov/pubmed/26949445
http://dx.doi.org/10.1155/2016/1543809
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