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Daunorubicin does not induce immunohistochemically detectable endothelial dysfunction in rabbit aorta and femoral artery

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dc.contributor.authorNachtigal, Petr
dc.contributor.authorŠterba, Martin
dc.contributor.authorPopelová, Olga
dc.contributor.authorVecerova, lenka
dc.contributor.authorKudláčková, Zdeňka
dc.contributor.authorJirkovský, Eduard
dc.contributor.authorGeršl, Vladimír
dc.date.accessioned2016-04-13T09:53:57Z
dc.date.available2016-04-13T09:53:57Z
dc.date.issued2011
dc.description.abstractAnthracyclines are one of the most effective anticancer drugs ever developed, but their clinical use has been hampered by the risk of severe cardiotoxicity. In this study, we investigated whether rabbits exposed to a different cumulative dose of anthracycline suffer from immunohistochemically detectable vascular toxicity and endothelial dysfunction. Daunorubicin (3 mg/kg, i.e. 50 mg/m2) was administered i.v. to rabbits once weekly for 1-10 weeks to reach different cumulative doses of the drug (50-500 mg/m2), while control rabbits received saline. The rabbits were sacrificed either 24 hours or 7 days after reaching each particular cumulative dose, and aortas and right femoral arteries were collected for immunohistochemical analysis. Immunohistochemical analysis showed ICAM-1 staining in many aortas from both saline and daunorubicin-treated rabbits without any relationship to the anthracycline treatment. On the contrary, unlike in the lipopolysaccharide-treated or hypercholesterolemic rabbits, no distinct immunoreactivity for other markers of inflammation, oxidative and nitrosative stress (VCAM-1, 4-HNE, iNOS and nitrotyrosine) were detected in aortas and femoral arteries from either control or daunorubicin-treated animals. No relationship to the cumulative dose of the drug or post-expose set up of harvesting was found. In this study, we have demonstrated that daunorubicin does not induce gross histopathological changes in the studied arteries and it fails to induce immunohistochemically detectable endothelial dysfunction. Thus, we propose that endothelial cells are much less susceptible to anthracycline toxicity than cardiac myocytes. In addition, our data suggest that vascular toxicity of anthracyclines plays rather a minor role in the cardiovascular complications of anthracycline chemotherapy.es
dc.formatapplication/pdfes
dc.format.extent12es
dc.identifier.issn1699-5848
dc.identifier.issn0213-3911
dc.identifier.urihttp://hdl.handle.net/10201/48560
dc.languageenges
dc.publisherMurcia: F. Hernándezes
dc.relation.ispartofHistology and Histopathology, vol. 26, nº 5, (2011)es
dc.rightsinfo:eu-repo/semantics/openAccesses
dc.subjectAnthracyclineses
dc.subjectEndothelial dysfunctiones
dc.subjectImmunohistochemistryes
dc.subject.other61 - Medicinaes
dc.titleDaunorubicin does not induce immunohistochemically detectable endothelial dysfunction in rabbit aorta and femoral arteryes
dc.typeinfo:eu-repo/semantics/articlees
dspace.entity.typePublicationes
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Histology and histopathology Vol.26, nº5 (2011)