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Age-associated changes in Ca(2+)-ATPase and oxidative damage in sarcoplasmic reticulum of rat heart
E. Babušíková, J. Lehotský, D. Dobrota, P. Račay, P. Kaplán
Jazyk angličtina Země Česko
Typ dokumentu časopisecké články, práce podpořená grantem
NLK
Directory of Open Access Journals
od 1991
Free Medical Journals
od 1998
ProQuest Central
od 2005-01-01
Medline Complete (EBSCOhost)
od 2006-01-01
Nursing & Allied Health Database (ProQuest)
od 2005-01-01
Health & Medicine (ProQuest)
od 2005-01-01
ROAD: Directory of Open Access Scholarly Resources
od 1998
- MeSH
- Ca2+-ATPasy metabolismus MeSH
- krysa rodu rattus MeSH
- kultivované buňky MeSH
- myokard enzymologie patologie MeSH
- oxidace-redukce MeSH
- oxidační stres fyziologie MeSH
- potkani Wistar MeSH
- sarkoplazmatické retikulum enzymologie MeSH
- stárnutí patologie fyziologie MeSH
- zvířata MeSH
- Check Tag
- krysa rodu rattus MeSH
- mužské pohlaví MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
Altered Ca(2+) handling may be responsible for the development of cardiac contractile dysfunctions with advanced age. In the present study, we investigated the roles of oxidative damage to sarcoplasmic reticulum (SR) and expression of Ca(2+)-ATPase (SERCA 2a) and phospholamban in age-associated dysfunction of cardiac SR. SR vesicles were prepared from hearts of 2-, 6-, 15-, and 26-month-old Wistar rats. Although activity of Ca(2+)-ATPase decreased with advancing age, no differences in relative amounts of SERCA 2a and phospholamban protein were observed. On the other hand, significant accumulation of protein oxidative damage occurred with aging. The results of this study suggest that age-related alteration in Ca(2+)-ATPase activity in the rat heart is not a consequence of decreased protein levels of SERCA 2a and phospholamban, but could arise from oxidative modifications of SR proteins. Cellular oxidative damage caused by reactive oxygen species could contribute to age-related alternations in myocardial relaxation.
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- $a Altered Ca(2+) handling may be responsible for the development of cardiac contractile dysfunctions with advanced age. In the present study, we investigated the roles of oxidative damage to sarcoplasmic reticulum (SR) and expression of Ca(2+)-ATPase (SERCA 2a) and phospholamban in age-associated dysfunction of cardiac SR. SR vesicles were prepared from hearts of 2-, 6-, 15-, and 26-month-old Wistar rats. Although activity of Ca(2+)-ATPase decreased with advancing age, no differences in relative amounts of SERCA 2a and phospholamban protein were observed. On the other hand, significant accumulation of protein oxidative damage occurred with aging. The results of this study suggest that age-related alteration in Ca(2+)-ATPase activity in the rat heart is not a consequence of decreased protein levels of SERCA 2a and phospholamban, but could arise from oxidative modifications of SR proteins. Cellular oxidative damage caused by reactive oxygen species could contribute to age-related alternations in myocardial relaxation.
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