title: Effect of iodothyronine hormone status on doxorubicin related cardiotoxicity.
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.
authors.forename: J
authors.initials: J
authors.lastname: Dudka
authors.forename: S
authors.initials: S
authors.lastname: Mandziuk
authors.forename: B
authors.initials: B
authors.lastname: Madej-Czerwonka
authors.forename: J
authors.initials: J
authors.lastname: Sierocińska-Sawa
authors.forename: B
authors.initials: B
authors.lastname: Walczyna
authors.forename: A
authors.initials: A
authors.lastname: Korga
authors.forename: M
authors.initials: M
authors.lastname: Cendrowska-Pinkosz
authors.affiliation: Experimental Teratology Unit, Human Anatomy Department, Medical University of Lublin. fb3@wp.pl.
authors.forename: F
authors.initials: F
authors.lastname: Burdan
mesh_terms: D000410:Alanine Transaminase / Q000097:blood; D000818:Animals; D001219:Aspartate Aminotransferases / Q000097:blood; D002318:Cardiovascular Diseases / Q000097:blood* / Q000139:chemically induced* / Q000201:enzymology; D003402:Creatine Kinase / Q000097:blood; D004317:Doxorubicin / Q000009:adverse effects*; D050556:Fatty Acid-Binding Proteins / Q000097:blood; D007770:L-Lactate Dehydrogenase / Q000097:blood; D008297:Male; D009206:Myocardium / Q000201:enzymology / Q000473:pathology; D020097:Natriuretic Peptide, Brain / Q000097:blood; D051381:Rats; D017208:Rats, Wistar; D013961:Thyroid Gland / Q000473:pathology; D013974:Thyroxine / Q000097:blood*; D014284:Triiodothyronine / Q000097:blood*; D019210:Troponin I / Q000378:metabolism
chemical_list: C493321:Fabp1 protein, rat; D050556:Fatty Acid-Binding Proteins; D019210:Troponin I; D014284:Triiodothyronine; D020097:Natriuretic Peptide, Brain; D004317:Doxorubicin; D007770:L-Lactate Dehydrogenase; D001219:Aspartate Aminotransferases; D000410:Alanine Transaminase; D003402:Creatine Kinase; D013974:Thyroxine