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The protection of the myocardium by amifostine against mitoxantrone-induced acute cardiotoxicity in rats

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dc.contributor.author Kadiköylü, V.G.
dc.contributor.author Meteoglu, I.
dc.contributor.author Demir, Süleyman
dc.contributor.author Aybek, Hülya
dc.contributor.author Kalak, M.
dc.contributor.author Balkaya, M.
dc.contributor.author Yenisey, Ç.
dc.date.accessioned 2019-08-16T12:06:24Z
dc.date.available 2019-08-16T12:06:24Z
dc.date.issued 2010
dc.identifier.issn 1300-7777
dc.identifier.uri https://hdl.handle.net/11499/6347
dc.identifier.uri https://doi.org/10.5152/tjh.2010.02
dc.description.abstract Objective: Amifostine (AMI) has been used for the prevention of doxorubicin-induced cardiotoxicity in several experimental and a few clinical studies. The aim of this study was to investigate the effects of AMI on lipid peroxidation, protective enzymes, and mitoxantrone (MITO)-induced acute cardiotoxicity in the rat heart using biochemical tests and histopatho-logical examinations. Materials and Methods: Thirty-six rats were divided into six groups (n=6 in each). Control rats were given intraperitoneal (i.p.) serum saline and AMI group rats were given 200 mg/kg AMI i.p. Rats received MITO-2.5 and 5 mg/kg i.p. in the MITO-2.5 and MITO-5 groups. AMI 200 mg/kg i.p. was administered 30 min. before the same doses of MITO in the MITO-2.5+AMI and MITO-5+AMI groups. Results: The levels of cardiac enzymes such as creatinine phosphokinase-myocardial band and cardiac troponin T did not change. Malondialdehyde (MDA) levels increased in MITO groups compared to controls. Catalase and glutathione (GSH) levels in the MITO and MITO+AMI groups were higher than in controls. Superoxide dismutase and glutathione peroxidase levels were not different between MITO groups and controls. There was no difference in MDA levels between MITO+AMI groups and controls. Calcium deposition was not detected. The scores of fibrosis, apoptosis, inflammation, and degeneration in MITO groups were higher than in controls. The scores of fibrosis, degeneration and inflammation in MITO+AMI groups were lower. Conclusion: MITO caused lipid peroxidation and myocardial damage, and the myocardium increased catalase and GSH levels to prevent this damage. AMI can protect against MITO-induced acute cardiotoxicity, decreasing myocardial damage and lipid peroxidation. en_US
dc.language.iso tr en_US
dc.relation.ispartof Turkish Journal of Hematology en_US
dc.rights info:eu-repo/semantics/openAccess en_US
dc.subject Acute cardiotoxicity en_US
dc.subject Amifostine en_US
dc.subject Lipid peroxidation en_US
dc.subject Mitoxantrone en_US
dc.subject amifostine en_US
dc.subject calcium en_US
dc.subject catalase en_US
dc.subject creatine kinase MB en_US
dc.subject glutathione en_US
dc.subject glutathione peroxidase en_US
dc.subject malonaldehyde en_US
dc.subject mitoxantrone en_US
dc.subject sodium chloride en_US
dc.subject superoxide dismutase en_US
dc.subject troponin T en_US
dc.subject acute disease en_US
dc.subject animal experiment en_US
dc.subject animal model en_US
dc.subject animal tissue en_US
dc.subject apoptosis en_US
dc.subject article en_US
dc.subject cardiotoxicity en_US
dc.subject controlled study en_US
dc.subject creatine kinase blood level en_US
dc.subject degeneration en_US
dc.subject enzyme blood level en_US
dc.subject fibrosis en_US
dc.subject heart protection en_US
dc.subject histopathology en_US
dc.subject inflammation en_US
dc.subject lipid peroxidation en_US
dc.subject male en_US
dc.subject nonhuman en_US
dc.subject protein blood level en_US
dc.subject rat en_US
dc.title The protection of the myocardium by amifostine against mitoxantrone-induced acute cardiotoxicity in rats en_US
dc.type Article en_US
dc.identifier.volume 27 en_US
dc.identifier.issue 2 en_US
dc.identifier.startpage 62
dc.identifier.startpage 62 en_US
dc.identifier.endpage 69 en_US
dc.identifier.doi 10.5152/tjh.2010.02
dc.relation.publicationcategory Makale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanı en_US
dc.identifier.pmid 27263446 en_US
dc.identifier.scopus 2-s2.0-77954740491 en_US
dc.identifier.trdizinid 107272 en_US
dc.identifier.wos WOS:000278947500002 en_US
dc.baslikedit $$başlıkdublike$$

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