open access

Vol 72, No 4 (2013)
ORIGINAL ARTICLES
Published online: 2013-12-10
Submitted: 2013-05-20
Accepted: 2013-06-07
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Effect of iodothyronine hormone status on doxorubicin related cardiotoxicity

J. Dudka, S. Mandziuk, B. Madej-Czerwonka, J. Sierocińska-Sawa, B. Walczyna, A. Korga, M. Cendrowska-Pinkosz, F. Burdan
DOI: 10.5603/FM.2013.0057
·
Folia Morphol 2013;72(4):340-348.

open access

Vol 72, No 4 (2013)
ORIGINAL ARTICLES
Published online: 2013-12-10
Submitted: 2013-05-20
Accepted: 2013-06-07

Abstract

The anthracycline anticancer agent doxorubicin has been recognised to induce a dose-dependent cardiotoxicity. The chronic form of such complication is characterized by an irreversible cardiac damage and congestive heart failure. Although the pathogenesis of anthracycline cardiotoxicity seems to be multifactorial, the pivotal role has been attributed to reactive oxygen species formation. Because redox equilibrium in cardiomyocytes may be regulated via iodothyronine hormones, the aim of the study was to appraise the effect of hypothyroidism on heart damages induced by doxorubicin. The rats received methimazole in drinking water (0.001 and 0.025%) after doxorubicin administration (2.0, 5.0 and 15 mg/kg). The cardiac morphology and blood biochemical markers of heart damage were assessed. Decreased levels of iodothyronine hormones had not significant impact on cardiac morphological changes and no effect on the level of B-type natriuretic peptide in rats receiving doxorubicin. Lower hormonal levels had sporadic, diverse effect on blood transaminases, lactate dehydrogenase and creatine kinase levels, but any relation to time, doxorubicin doses and hypothyroid status was found. Hypothyreosis leads to increase in fatty acid binding protein in rats receiving higher dose of doxorubicin. Hypothyreosis had no effect on heart stretching and on necrosis at morphological level, but caused biochemical symptoms of cardiomyocyte necrosis in rats receiving doxorubicin.

Abstract

The anthracycline anticancer agent doxorubicin has been recognised to induce a dose-dependent cardiotoxicity. The chronic form of such complication is characterized by an irreversible cardiac damage and congestive heart failure. Although the pathogenesis of anthracycline cardiotoxicity seems to be multifactorial, the pivotal role has been attributed to reactive oxygen species formation. Because redox equilibrium in cardiomyocytes may be regulated via iodothyronine hormones, the aim of the study was to appraise the effect of hypothyroidism on heart damages induced by doxorubicin. The rats received methimazole in drinking water (0.001 and 0.025%) after doxorubicin administration (2.0, 5.0 and 15 mg/kg). The cardiac morphology and blood biochemical markers of heart damage were assessed. Decreased levels of iodothyronine hormones had not significant impact on cardiac morphological changes and no effect on the level of B-type natriuretic peptide in rats receiving doxorubicin. Lower hormonal levels had sporadic, diverse effect on blood transaminases, lactate dehydrogenase and creatine kinase levels, but any relation to time, doxorubicin doses and hypothyroid status was found. Hypothyreosis leads to increase in fatty acid binding protein in rats receiving higher dose of doxorubicin. Hypothyreosis had no effect on heart stretching and on necrosis at morphological level, but caused biochemical symptoms of cardiomyocyte necrosis in rats receiving doxorubicin.

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Keywords

doxorubicin, cardiotoxicity, hypothyreosis

About this article
Title

Effect of iodothyronine hormone status on doxorubicin related cardiotoxicity

Journal

Folia Morphologica

Issue

Vol 72, No 4 (2013)

Pages

340-348

Published online

2013-12-10

DOI

10.5603/FM.2013.0057

Bibliographic record

Folia Morphol 2013;72(4):340-348.

Keywords

doxorubicin
cardiotoxicity
hypothyreosis

Authors

J. Dudka
S. Mandziuk
B. Madej-Czerwonka
J. Sierocińska-Sawa
B. Walczyna
A. Korga
M. Cendrowska-Pinkosz
F. Burdan

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