Literature DB >> 14767771

Partial and delayed release of troponin-I compared with the release of lactate dehydrogenase from necrotic cardiomyocytes.

Lijuan Li1, Marleen Hessel, Lizet van der Valk, Minka Bax, Irma van der Linden, Arnoud van der Laarse.   

Abstract

Although the troponins are the serum proteins most frequently used nowadays to diagnose myocardial infarction, controversy continues about whether troponins are released later from infarcted myocardium than the cytoplasmic enzymes used previously, like lactate dehydrogenase (LDH). The present study compared the release kinetics of troponin-I (TnI) and LDH from necrotic cardiomyocytes in vitro. Cardiomyocytes prepared from neonatal rat ventricles were grown for 3 days. A total of 126 cultures were subjected to metabolic inhibition to induce cell necrosis. At various time intervals cells and media were collected for quantitative analysis of LDH activity and TnI concentration. Mean (+/-SD) LDH activity and TnI content of nine cultures at time t=0 were 2.07+/-0.30 U and 1.52+/-0.30 micro g per culture, respectively. Release of LDH from necrotic cardiomyocytes preceded release of TnI by about 60 min. The quantity of LDH released from the cultures after 210 min was 83.2+/-10.0%, whereas that of TnI released after 210 min was always less (33.8+/-22.2%). Cytochemical assessment of necrotic cardiomyocytes showed TnI-positive cells that were poor in LDH. The delay of TnI release relative to LDH release may be explained by slow dissociation of TnI molecules from myofilaments and/or formation of TnI degradation products that are undetected by the currently used ELISA assay.

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Year:  2004        PMID: 14767771     DOI: 10.1007/s00424-003-1236-3

Source DB:  PubMed          Journal:  Pflugers Arch        ISSN: 0031-6768            Impact factor:   3.657


  33 in total

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7.  Integrin stimulation-induced hypertrophy in neonatal rat cardiomyocytes is NO-dependent.

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  7 in total

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