The protective effect of melatonin on adriamycin-induced acute cardiac injury

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dc.authoridHAYRAN, HATiCE Mürvet/0000-0001-6058-6304
dc.authorwosidHAYRAN, HATiCE Mürvet/I-8346-2013
dc.contributor.authorKoçak, G
dc.contributor.authorErbil, KM
dc.contributor.authorÖzdemir, I
dc.contributor.authorAydemir, S
dc.contributor.authorSunar, B
dc.contributor.authorTuncel, M
dc.contributor.authorAtalay, S
dc.date.accessioned2024-08-04T20:13:18Z
dc.date.available2024-08-04T20:13:18Z
dc.date.issued2003
dc.departmentİnönü Üniversitesien_US
dc.description.abstractBACKGROUND: Cardiotoxicity is the main complication of adriamycin (ADR), which is a widely used chemotherapeutic agent. OBJECTIVE: To examine the potential cardioprotective effect of melatonin (MEL) on acute ADR cardiotoxicity in a rat model. METHODS: Cardioprotection was assessed on the basis of myocardial lipid peroxidation and ultrastructure. Rats were given MEL at a daily dose of 5 mg/kg and ADR 15 mg/kg, intraperitoneally. The MEL-1 group rats received one dose and the MEL-7 group rats six daily doses of MEL and were sacrificed at the end of one and seven days, respectively. Rats in the ADR-1 and ADR-7 groups were each given a single dose of ADR, and were then sacrificed 24 h and seven days later, respectively. The MEL+ADR-1 group rats received one dose each of ADR and MEL simultaneously and were sacrificed 24 h later. The MEL+ADR-7 group received a single dose of ADR plus a daily MEL dose for six consecutive days, and were sacrificed seven days after the ADR injection. RESULTS: Lipid peroxidation products were elevated in both ADR-1 and ADR-7 groups, and this elevation was significantly inhibited by MEL treatment. Electron microscopy confirmed that ADR was positively cardiotoxic after one and seven days of exposure. The extent of ADR-induced myocardial damage was markedly reduced when MEL was combined with ADR (MEL+ADR-1 and MEL+ADR-7). CONCLUSION: The results suggest that MEL is highly efficacious at reducing the acute cardiotoxic effects of high dose ADR, and that it acts by preventing lipid peroxidation.en_US
dc.identifier.endpage541en_US
dc.identifier.issn0828-282X
dc.identifier.issn1916-7075
dc.identifier.issue5en_US
dc.identifier.pmid12717489en_US
dc.identifier.scopus2-s2.0-0037675177en_US
dc.identifier.scopusqualityQ1en_US
dc.identifier.startpage535en_US
dc.identifier.urihttps://hdl.handle.net/11616/93529
dc.identifier.volume19en_US
dc.identifier.wosWOS:000182446600009en_US
dc.identifier.wosqualityQ2en_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakScopusen_US
dc.indekslendigikaynakPubMeden_US
dc.language.isoenen_US
dc.publisherElsevier Science Incen_US
dc.relation.ispartofCanadian Journal of Cardiologyen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectadriamycinen_US
dc.subjectcardiotoxicityen_US
dc.subjectelectron microscopyen_US
dc.subjectfree radicalsen_US
dc.subjectmelatoninen_US
dc.titleThe protective effect of melatonin on adriamycin-induced acute cardiac injuryen_US
dc.typeArticleen_US

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