N-acetylcysteine treatment prevents the up-regulation of MnSOD in chronically hypoxic rat hearts
Jazyk angličtina Země Česko Médium print-electronic
Typ dokumentu časopisecké články
PubMed
21401304
DOI
10.33549/physiolres.932042
PII: 932042
Knihovny.cz E-zdroje
- MeSH
- acetylcystein farmakologie terapeutické užití MeSH
- hypoxie * MeSH
- krysa rodu Rattus MeSH
- mitochondrie metabolismus MeSH
- myokard metabolismus MeSH
- potkani Wistar MeSH
- reaktivní formy kyslíku metabolismus MeSH
- reperfuzní poškození myokardu metabolismus prevence a kontrola MeSH
- scavengery volných radikálů farmakologie terapeutické užití MeSH
- superoxiddismutasa genetika metabolismus MeSH
- upregulace * MeSH
- zvířata MeSH
- Check Tag
- krysa rodu Rattus MeSH
- mužské pohlaví MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- Názvy látek
- acetylcystein MeSH
- reaktivní formy kyslíku MeSH
- scavengery volných radikálů MeSH
- superoxiddismutasa MeSH
Chronic intermittent hypoxia (CIH) is associated with increased production of reactive oxygen species that contributes to the adaptive mechanism underlying the improved myocardial ischemic tolerance. The aim was to find out whether the antioxidative enzyme manganese superoxide dismutase (MnSOD) can play a role in CIH-induced cardioprotection. Adult male Wistar rats were exposed to intermittent hypobaric hypoxia (7000 m, 8 h/day, 25 exposures) (n=14) or kept at normoxia (n=14). Half of the animals from each group received N-acetylcysteine (NAC, 100 mg/kg) daily before the hypoxic exposure. The activity and expression of MnSOD were increased by 66 % and 23 %, respectively, in the mitochondrial fraction of CIH hearts as compared with the normoxic group; these effects were suppressed by NAC treatment. The negative correlation between MnSOD activity and myocardial infarct size suggests that MnSOD can contribute to the improved ischemic tolerance of CIH hearts.
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