RT info:eu-repo/semantics/article
T1 The effects of intermittent hypoxia on redox status, NF-κB activation, and plasma lipid levels are dependent on the lowest oxygen saturation
A1 Quintero, Miguel
A1 González-Martin, MC
A1 Vega-Agapito, Victoria
A1 Gonzalez, C
A1 Obeso, A
A1 Farré, R
A1 Agapito, MT
A1 Yubero, S
K1 Intermittent hypoxia, Oxidative stress, Free radicals
AB during sleep, causing concomitant episodes of systemic hypoxia and associated cardiovascular andmetabolic pathologies. The mechanisms generating these pathologies are controversial. Because recurrenthypoxia is the element of inadequate respiration that leads to the pathology, experimental models of OSASconsist in the exposure of the animals to intermittent hypoxia (IH) by cycling O2 percentages in theirhabitats. A proposed mechanism linking the IH of OSAS to pathologies is the increased production ofreactive oxygen species (ROS). However, it has been argued that many patients seem to lack oxidativestress and that, to augment ROS in IH animals, intense hypoxia, seldom encountered in patients, has to beapplied. 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 lipidperoxide levels, aconitase and fumarase activities, and ROS-disposal enzyme activity in liver, brain, andlung. Liver levels of nuclear NF-κB-p65 and plasma C-reactive protein (CRP), as well as lipid levels, werealso assessed. Lowest hemoglobin saturations were 91.770.8 and 73.571.4%. IH caused tissue-specificoxidative stress related to hypoxic intensity. Nuclear NF-κB-p65 and lipid content in the liver and CRP inthe plasma all increased with IH intensity, as did both plasma triglycerides and cholesterol. We concludethat IH, even of moderate intensity, causes oxidative stress probably related to the pathologies encounteredin OSAS patients.
PB Elsevier
YR 2013
FD 2013-12
LK https://uvadoc.uva.es/handle/10324/65611
UL https://uvadoc.uva.es/handle/10324/65611
LA eng
NO Free Radical Biology and Medicine, diciembre 2013,vol. 65, p.1143-1154
NO Producción Científica
DS UVaDOC
RD 27-dic-2024