N-acetylcysteine treatment prevents the up-regulation of MnSOD in chronically hypoxic rat hearts
Language English Country Czech Republic Media print-electronic
Document type Journal Article
PubMed
21401304
DOI
10.33549/physiolres.932042
PII: 932042
Knihovny.cz E-resources
- MeSH
- Acetylcysteine pharmacology therapeutic use MeSH
- Hypoxia * MeSH
- Rats MeSH
- Mitochondria metabolism MeSH
- Myocardium metabolism MeSH
- Rats, Wistar MeSH
- Reactive Oxygen Species metabolism MeSH
- Myocardial Reperfusion Injury metabolism prevention & control MeSH
- Free Radical Scavengers pharmacology therapeutic use MeSH
- Superoxide Dismutase genetics metabolism MeSH
- Up-Regulation * MeSH
- Animals MeSH
- Check Tag
- Rats MeSH
- Male MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Names of Substances
- Acetylcysteine MeSH
- Reactive Oxygen Species MeSH
- Free Radical Scavengers MeSH
- Superoxide Dismutase 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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