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001-es BibID:	BIBFORM005170
Első szerző:	Hertelendi Zita (orvos)
Cím:	The peroxynitrite evoked contractile depression can be partially reversed by antioxidants in human cardiomyocytes / Zita Hertelendi, Attila Tóth, Attila Borbély, Zoltán Galajda, István Édes, Árpád Tósaki, Zoltán Papp
Dátum:	2009
ISSN:	1582-1838 (Print)
Megjegyzések:	In this study, we aimed to determine the contribution of peroxynitrite-dependent sulfhydryl group (SH) oxidation to the contractile dysfunction in permeabilized left ventricular human cardiomyocytes using a comparative approach with the SH-oxidant 2,2'-dithiodipyridine (DTDP). Additionally, different antioxidants: dithiothreitol (DTT), reduced glutathione (GSH) or N-acetyl-L-cysteine (NAC) were employed to test reversibility. Maximal isometric active force production (F(o)) and the maximal turnover rate of the cross-bridge cycle (k(tr,max)) illustrated cardiomyocyte mechanics. SH oxidation was monitored by a semi-quantitative Ellman's assay and by SH-specific protein biotinylation. Both peroxynitrite and DTDP diminished F(o) in a concentration-dependent manner (EC(50,peroxynitrite) = 49 microM; EC(50,DTDP) = 2.75 mM). However, k(tr,max) was decreased only by 2.5-mM DTDP, but not by 50 microM peroxynitrite. The diminution of F(o) to zero by DTDP was paralleled by the complete elimination of the free SH groups, while the peroxynitrite-induced maximal reduction in free SH groups was only to 58 +/- 6% of the control (100%). The diminutions in F(o) and free SH groups evoked by 2.5-mM DTDP were completely reverted by DTT. In contrast, DTT induced only a partial restoration in F(o) (DeltaF(o,): approximately 13%; P < 0.05) despite full reversion in protein SH content after 50 microM peroxynitrite. Although, NAC or DTT were equally effective on F(o) after peroxynitrite exposures, NAC or GSH did not restore F(o) or k(tr,max) after DTDP treatments. Our results revealed that the peroxynitrite-evoked cardiomyocyte dysfunction has a small, but significant component resulting from reversible SH oxidation, and thereby illustrated the potential benefit of antioxidants during cardiac pathologies with excess peroxynitrite production.
Tárgyszavak:	Orvostudományok Gyógyszerészeti tudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:	Journal of Cellular and Molecular Medicine. - 13 : 8B (2009), p. 2200-2209. -
További szerzők:	Tóth Attila (1971-) (biológus) Borbély Attila (1978-) (kardiológus) Galajda Zoltán (1962-) (szívsebész, érsebész) Édes István (1952-) (kardiológus) Tósaki Árpád (1958-) (kísérletes farmakológus, gyógyszerész) Papp Zoltán (1965-) (kardiológus, élettanász)
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001-es BibID:	BIBFORM005640
Első szerző:	Sanganalmath, Santosh K.
Cím:	Antiplatelet therapy attenuates subcellular remodelling in congestive heart failure / Sanganalmath, S. K., Babick, A. P., Barta, J., Kumamoto, H., Takeda, N., Dhalla, N. S.
Dátum:	2008
ISSN:	1582-1838 (Print)
Megjegyzések:	Antiplatelet agents, sarpogrelate (SAR), a 5-HT(2A) receptor antagonist, and cilostazol (CIL), a phosphodiesterase III (PDE-III) inhibitor, are used for the treatment of peripheral vascular disease. We tested whether these agents affect cardiac function and subcellular remodelling in congestive heart failure (CHF) induced by myocardial infarction (MI). Three weeks after MI, rats were treated daily with 5 mg/kg SAR or CIL as well as vehicle for 5 weeks. Sham-operated animals served as controls. At end of the treatment period, haemodynamic measurements were performed and the left ventricle was processed for the determination of sarcoplasmic reticulum (SR) Ca(2+)-uptake and -release activities, and expression of SR Ca(2+)-pump, phospholamban and ryanodine receptors, as well as myofibrillar ATPase activities, expression of alpha- and beta-myosin heavy chain (MHC) isoforms, and phosphorylation of phospholamban and cardiac troponin-I (c Tn-I). Marked haemodynamic changes in the MI-induced CHF were associated with depressions in SR Ca (+)-uptake and -release activities as well as in protein content and gene expression for SR proteins. Furthermore, myofibrillar Ca(2+)-stimulated ATPase activity, as well as protein content and gene expression for alpha-MHC were decreased whereas those for beta-MHC were increased in the failing heart. Also, phosphorylation levels of phospholamban and cTn-I were reduced in failing hearts. The MI-associated changes in cardiac function, SR and myofibillar activities, as well as SR and myofibrillar protein and gene expression were attenuated by treatment with SAR or CIL. The results suggest that SAR and CIL improve cardiac function by ameliorating subcellular remodelling in the failing heart and indicate the potential therapy of CHF with antiplatelet agents.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban Adenosine Triphosphatases/metabolism Animals Blood Platelets Calcium/metabolism Gene Expression Regulation Heart Failure/genetics/metabolism/surgery/ therapy Hemodynamics Male Myosin Heavy Chains/metabolism Protein Isoforms/metabolism Proteins/genetics/metabolism RNA, Messenger/genetics Rats Rats, Sprague-Dawley Sarcoplasmic Reticulum/metabolism Subcellular Fractions/metabolism
Megjelenés:	Journal of Cellular and Molecular Medicine. - 12 : 5A (2008), p. 1728-1738. -
További szerzők:	Babick, Andrea P. Barta Judit (1975-) (kardiológus) Kumamoto, Hideo Takeda, Nobuakiya Dhalla, Naranjan S.
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