Cardiac troponin T as a marker of myocardial damage caused by antineoplastic drugs in rabbits

Citation
M. Adamcova et al., Cardiac troponin T as a marker of myocardial damage caused by antineoplastic drugs in rabbits, J CANC RES, 125(5), 1999, pp. 268-274
Citations number
39
Categorie Soggetti
Onconogenesis & Cancer Research
Journal title
JOURNAL OF CANCER RESEARCH AND CLINICAL ONCOLOGY
ISSN journal
01715216 → ACNP
Volume
125
Issue
5
Year of publication
1999
Pages
268 - 274
Database
ISI
SICI code
0171-5216(199905)125:5<268:CTTAAM>2.0.ZU;2-F
Abstract
Anthracycline derivatives are among the most effective antineoplastic drugs but their therapeutic use is limited by their adverse effects. The cardiac side-effects of antineoplastic drugs were investigated in rabbits in vivo from the viewpoint of release of cardiac troponin T (cTnT) measured by Elec sys Troponin T STAT immunoassay (Boehringer Mannheim, Germany). No increase in cTnT was found following administration of a single dose of daunorubici n (3 mg/kg i.v., n = 4). During development of daunorubicin-induced cardiom yopathy (daunorubicin 3 mg/kg i.v., once a week; maximum nine administratio ns, n = 7), the levels of cTnT were within the physiological range (i.e. cT nT < 0.1 mu g/l) at the beginning of the experiment and before and after th e 5th administration, but the pathological values of cTnT after the 8th adm inistration in 43% animals (0.22 +/- 0.08 mu g/l) correlated with their pre mature death. In the control group, the levels of cTnT were always lower th an 0.1 mu g/l during the experiment. Following administration of a new anti neoplastic drug - Oracin {6-[2-(2-hydroxyethyl) aminoethyl]-5,11-dioxo-5,6- dihydro-11H-indeno [1,2-c]-isoquinoline hydrothloride, 10 mg/kg i.v., once weekly, ten administrations, n = 7}, there was no increase in cTnT levels. These findings correlated with the PEP: LVET index, histological examinatio n and no animal succumbing to premature death. It is possible to conclude t hat cTnT is a useful marker for the prediction of experimentally induced an thracycline cardiomyopathy and for the evaluation of cardiotoxic (and, poss ibly, cardioprotective) effects of new drugs in rabbits.