Cardioprotective and nonprotective regimens of chronic hypoxia diversely affect the myocardial antioxidant systems
The result's identifiers
Result code in IS VaVaI
<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F75010330%3A_____%2F15%3A00011092" target="_blank" >RIV/75010330:_____/15:00011092 - isvavai.cz</a>
Alternative codes found
RIV/67985823:_____/15:00451957 RIV/00216208:11310/15:10316367
Result on the web
<a href="http://physiolgenomics.physiology.org/content/47/12/612" target="_blank" >http://physiolgenomics.physiology.org/content/47/12/612</a>
DOI - Digital Object Identifier
<a href="http://dx.doi.org/10.1152/physiolgenomics.00058.2015" target="_blank" >10.1152/physiolgenomics.00058.2015</a>
Alternative languages
Result language
angličtina
Original language name
Cardioprotective and nonprotective regimens of chronic hypoxia diversely affect the myocardial antioxidant systems
Original language description
It has been documented that adaptation to hypoxia increases myocardial tolerance to ischemia-reperfusion (I/R) injury depending on the regimen of adaptation. Reactive oxygen species (ROS) formed during hypoxia play an important role in the induction of protective cardiac phenotype. On the other hand, the excess of ROS can contribute to tissue damage caused by I/R. Here we investigated the relationship between myocardial tolerance to I/R injury and transcription activity of major antioxidant genes, transcription factors, and oxidative stress in three different regimens of chronic hypoxia. Adult male Wistar rats were exposed to continuous normobaric hypoxia (FIO2 0.1) either continuously (CNH) or intermittently for 8 h/day (INH8) or 23 h/day (INH23) for 3 wk period. A control group was kept in room air. Myocardial infarct size was assessed in anesthetized open-chest animals subjected to 20 min coronary artery occlusion and 3 h reperfusion. Levels of mRNA transcripts and the ratio of reduced and oxidized glutathione (GSH/GSSG) were analyzed by real-time RT-PCR and by liquid chromatography, respectively. Whereas CNH as well as INH8 decreased infarct size, 1 h daily reoxygenation (INH23) abolished the cardioprotective effect and decreased GSH/GSSG ratio. The majority of mRNAs of antioxidant genes related to mitochondrial antioxidant defense (manganese superoxide dismutase, glutathione reductase, thioredoxin/thioredoxin reductase, and peroxiredoxin 2) were upregulated in both cardioprotective regimens (CNH, INH8). In contrast, INH23 increased only PRX5, which was not sufficient to induce the cardioprotective phenotype. Our results suggest that the increased mitochondrial antioxidant defense plays an important role in cardioprotection afforded by chronic hypoxia.
Czech name
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Czech description
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Classification
Type
J<sub>x</sub> - Unclassified - Peer-reviewed scientific article (Jimp, Jsc and Jost)
CEP classification
FA - Cardiovascular diseases including cardio-surgery
OECD FORD branch
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Result continuities
Project
Result was created during the realization of more than one project. More information in the Projects tab.
Continuities
V - Vyzkumna aktivita podporovana z jinych verejnych zdroju
Others
Publication year
2015
Confidentiality
S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů
Data specific for result type
Name of the periodical
Physiological Genomics
ISSN
1094-8341
e-ISSN
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Volume of the periodical
47
Issue of the periodical within the volume
12
Country of publishing house
US - UNITED STATES
Number of pages
9
Pages from-to
612-620
UT code for WoS article
000365900400004
EID of the result in the Scopus database
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