The effects of intermittent hypoxia on redox status, NF-κB activation, and plasma lipid levels are dependent on the lowest oxygen saturation

Producción Científica

Detalles Bibliográficos
Autores: Quintero, Miguel, González-Martin, MC, Vega Agapito, María Victoria, González Martínez, Constancio, Obeso Cáceres, Ana María de la Luz, Farré, R, Agapito Serrano, María Teresa, Yubero Benito, Sara
Tipo de recurso: artículo
Estado:Versión publicada
Fecha de publicación:2013
País:España
Institución:Universidad de Valladolid
Repositorio:UVaDOC. Repositorio Documental de la Universidad de Valladolid
OAI Identifier:oai:uvadoc.uva.es:10324/65611
Acceso en línea:https://doi.org/10.1016/j.freeradbiomed.2013.08.180
https://uvadoc.uva.es/handle/10324/65611
Access Level:acceso abierto
Palabra clave:Intermittent hypoxia, Oxidative stress, Free radicals
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spelling The effects of intermittent hypoxia on redox status, NF-κB activation, and plasma lipid levels are dependent on the lowest oxygen saturationQuintero, MiguelGonzález-Martin, MCVega Agapito, María VictoriaGonzález Martínez, ConstancioObeso Cáceres, Ana María de la LuzFarré, RAgapito Serrano, María TeresaYubero Benito, SaraIntermittent hypoxia, Oxidative stress, Free radicalsProducción Científicaduring sleep, causing concomitant episodes of systemic hypoxia and associated cardiovascular and metabolic pathologies. The mechanisms generating these pathologies are controversial. Because recurrent hypoxia is the element of inadequate respiration that leads to the pathology, experimental models of OSAS consist in the exposure of the animals to intermittent hypoxia (IH) by cycling O2 percentages in their habitats. A proposed mechanism linking the IH of OSAS to pathologies is the increased production of reactive oxygen species (ROS). However, it has been argued that many patients seem to lack oxidative stress and that, to augment ROS in IH animals, intense hypoxia, seldom encountered in patients, has to be applied. To solve the controversy, we have exposed rats to two intensities of IH (cycles of 10 or 5% O2, 40 s, and then 21% O2, 80 s; 8 h/day, 15 days). We then measured reduced and oxidized glutathione and lipid peroxide levels, aconitase and fumarase activities, and ROS-disposal enzyme activity in liver, brain, and lung. Liver levels of nuclear NF-κB-p65 and plasma C-reactive protein (CRP), as well as lipid levels, were also assessed. Lowest hemoglobin saturations were 91.770.8 and 73.571.4%. IH caused tissue-specific oxidative stress related to hypoxic intensity. Nuclear NF-κB-p65 and lipid content in the liver and CRP in the plasma all increased with IH intensity, as did both plasma triglycerides and cholesterol. We conclude that IH, even of moderate intensity, causes oxidative stress probably related to the pathologies encountered in OSAS patients.Este trabajo fue financiado por Spanish Ministry of Science and Innovation (Grants BFU2007-61848 to Constancio Gonzalez and SAF2011-22576 to Ramon Farre); the Spanish Ministry of Economy and Competitiveness (Grant BFU2012-37459 to Constancio Gonzalez), and the Spanish Ministry of Health–Institute Carlos III (Grant CIBER CB06/06/0050 to Constancio Gonzalez and Ramón Farre).Elsevier2013info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionapplication/pdfhttps://doi.org/10.1016/j.freeradbiomed.2013.08.180https://uvadoc.uva.es/handle/10324/65611reponame:UVaDOC. Repositorio Documental de la Universidad de Valladolidinstname:Universidad de ValladolidIngléshttps://www.sciencedirect.com/science/article/pii/S0891584913005832?via%3Dihubinfo:eu-repo/semantics/openAccessoai:uvadoc.uva.es:10324/656112026-06-13T12:44:47Z
dc.title.none.fl_str_mv The effects of intermittent hypoxia on redox status, NF-κB activation, and plasma lipid levels are dependent on the lowest oxygen saturation
title The effects of intermittent hypoxia on redox status, NF-κB activation, and plasma lipid levels are dependent on the lowest oxygen saturation
spellingShingle The effects of intermittent hypoxia on redox status, NF-κB activation, and plasma lipid levels are dependent on the lowest oxygen saturation
Quintero, Miguel
Intermittent hypoxia, Oxidative stress, Free radicals
title_short The effects of intermittent hypoxia on redox status, NF-κB activation, and plasma lipid levels are dependent on the lowest oxygen saturation
title_full The effects of intermittent hypoxia on redox status, NF-κB activation, and plasma lipid levels are dependent on the lowest oxygen saturation
title_fullStr The effects of intermittent hypoxia on redox status, NF-κB activation, and plasma lipid levels are dependent on the lowest oxygen saturation
title_full_unstemmed The effects of intermittent hypoxia on redox status, NF-κB activation, and plasma lipid levels are dependent on the lowest oxygen saturation
title_sort The effects of intermittent hypoxia on redox status, NF-κB activation, and plasma lipid levels are dependent on the lowest oxygen saturation
dc.creator.none.fl_str_mv Quintero, Miguel
González-Martin, MC
Vega Agapito, María Victoria
González Martínez, Constancio
Obeso Cáceres, Ana María de la Luz
Farré, R
Agapito Serrano, María Teresa
Yubero Benito, Sara
author Quintero, Miguel
author_facet Quintero, Miguel
González-Martin, MC
Vega Agapito, María Victoria
González Martínez, Constancio
Obeso Cáceres, Ana María de la Luz
Farré, R
Agapito Serrano, María Teresa
Yubero Benito, Sara
author_role author
author2 González-Martin, MC
Vega Agapito, María Victoria
González Martínez, Constancio
Obeso Cáceres, Ana María de la Luz
Farré, R
Agapito Serrano, María Teresa
Yubero Benito, Sara
author2_role author
author
author
author
author
author
author
dc.subject.none.fl_str_mv Intermittent hypoxia, Oxidative stress, Free radicals
topic Intermittent hypoxia, Oxidative stress, Free radicals
description Producción Científica
publishDate 2013
dc.date.none.fl_str_mv 2013
dc.type.none.fl_str_mv info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
format article
status_str publishedVersion
dc.identifier.none.fl_str_mv https://doi.org/10.1016/j.freeradbiomed.2013.08.180
https://uvadoc.uva.es/handle/10324/65611
url https://doi.org/10.1016/j.freeradbiomed.2013.08.180
https://uvadoc.uva.es/handle/10324/65611
dc.language.none.fl_str_mv Inglés
language_invalid_str_mv Inglés
dc.relation.none.fl_str_mv https://www.sciencedirect.com/science/article/pii/S0891584913005832?via%3Dihub
dc.rights.none.fl_str_mv info:eu-repo/semantics/openAccess
eu_rights_str_mv openAccess
dc.format.none.fl_str_mv application/pdf
dc.publisher.none.fl_str_mv Elsevier
publisher.none.fl_str_mv Elsevier
dc.source.none.fl_str_mv reponame:UVaDOC. Repositorio Documental de la Universidad de Valladolid
instname:Universidad de Valladolid
instname_str Universidad de Valladolid
reponame_str UVaDOC. Repositorio Documental de la Universidad de Valladolid
collection UVaDOC. Repositorio Documental de la Universidad de Valladolid
repository.name.fl_str_mv
repository.mail.fl_str_mv
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score 15,301603

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