Protective effects of erdosteine against doxorubicin-induced cardiomyopathy in rats

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dc.authorwosidFadillioglu, Ersin/K-3817-2019
dc.authorwosidErdogan, Hasan/AFN-9249-2022
dc.contributor.authorFadillioglu, E
dc.contributor.authorErdogan, H
dc.contributor.authorSögüt, S
dc.contributor.authorKuku, I
dc.date.accessioned2024-08-04T20:13:36Z
dc.date.available2024-08-04T20:13:36Z
dc.date.issued2003
dc.departmentİnönü Üniversitesien_US
dc.description2nd International Meeting on Free Radicals in Health and Disease -- MAY 08-12, 2002 -- ISTANBUL, TURKEYen_US
dc.description.abstractThe usefulness of doxorubicin (DXR) is limited by its cardiotoxicity. In order to improve future DXR therapy by using a new antioxidant agent, an experimental study was designed. This study was undertaken to determine whether DXR-induced cardiotoxicity is prevented by erdosteine, a mucolytic agent showing antioxidant properties. Three groups of male Sprague-Dawley rats (60 days old) were used: one group was untreated as a control; the other groups were treated with DXR (single i.p. dosage of 20 mg kg(-1) body wt.) or DXR plus erdosteine (10 mg kg(-1) day(-1), orally), respectively. The DXR treatment without erdosteine increased antioxidant enzyme activities and also increased lipid peroxidation in myocardial tissue. The rats treated with DXR plus erdosteine produced a significant decrease in lipid peroxidation in comparison with control and DXR groups. Furthermore, erdosteine administration led to an increase in antioxidant enzyme activities in comparison with the control group. Erdosteine treatment also increased the activities of catalase (CAT) and glutathione peroxidase (GSH-Px) in comparison with the DXR group. There was no significant difference in lipid peroxidation of myocardial tissue between control and DXR plus erdosteine-treated rats. It was concluded that erdosteine caused an increase in the activities of antioxidant enzymes, especially GSH-Px and CAT, protecting the heart tissue sufficiently from oxidative damage to membrane lipids and other cellular components induced by DXR. Copyright (C) 2003 John Wiley Sons, Ltd.en_US
dc.identifier.doi10.1002/jat.889
dc.identifier.endpage74en_US
dc.identifier.issn0260-437X
dc.identifier.issn1099-1263
dc.identifier.issue1en_US
dc.identifier.pmid12518339en_US
dc.identifier.scopus2-s2.0-0347722762en_US
dc.identifier.scopusqualityQ2en_US
dc.identifier.startpage71en_US
dc.identifier.urihttps://doi.org/10.1002/jat.889
dc.identifier.urihttps://hdl.handle.net/11616/93717
dc.identifier.volume23en_US
dc.identifier.wosWOS:000180728600010en_US
dc.identifier.wosqualityQ3en_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakScopusen_US
dc.indekslendigikaynakPubMeden_US
dc.language.isoenen_US
dc.publisherWileyen_US
dc.relation.ispartofJournal of Applied Toxicologyen_US
dc.relation.publicationcategoryKonferans Öğesi - Uluslararası - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectdoxorubicinen_US
dc.subjecterdosteineen_US
dc.subjectcardiotoxicityen_US
dc.subjectoxidantsen_US
dc.subjectantioxidantsen_US
dc.subjectlipid peroxidationen_US
dc.subjectcatalaseen_US
dc.subjectsuperoxide dismutaseen_US
dc.subjectglutathione peroxidaseen_US
dc.titleProtective effects of erdosteine against doxorubicin-induced cardiomyopathy in ratsen_US
dc.typeConference Objecten_US

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