Effects of Fullerenol C60(OH)24 Nanoparticles on a Single-dose Doxorubicin-induced Cardiotoxicity in Pigs: An Ultrastructural Study
Autor: | Mariana Seke, Ivana Icevic, Zdenko Kanacki, Aleksandar Djordjevic, Milica Labudovic Borovic, Dragan Žikić, Rade Injac |
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Jazyk: | angličtina |
Rok vydání: | 2014 |
Předmět: |
Heart Diseases
Sus scrofa cardiotoxicity Pharmacology doxorubicin Pathology and Forensic Medicine 03 medical and health sciences 0302 clinical medicine Microscopy Electron Transmission Structural Biology Edema Parenchyma medicine Animals Myocytes Cardiac Doxorubicin fullerenol nanoparticles 030304 developmental biology Cardiomyocytes 0303 health sciences Cardiotoxicity Antibiotics Antineoplastic Chemistry Anatomy 3. Good health Vacuolization 030220 oncology & carcinogenesis Ultrastructure Nanoparticles Fullerenes medicine.symptom mitotic figures Myofibril Intracellular medicine.drug |
Zdroj: | Ultrastructural Pathology |
ISSN: | 0191-3123 |
DOI: | 10.3109/01913123.2013.822045 |
Popis: | Cardioprotective effects of fullerenol C-60(OH)(24) nanoparticles (FNP) were investigated in pigs after a single treatment with doxorubicin (DOX). Semithin and ultrathin sections of myocardial tissue routinely prepared for transmission electron microscopy were analyzed. Extensive intracellular damage was confirmed in cardiomyocytes of DOX-treated animals. By means of ultrastructural analysis, a certain degree of parenchymal degeneration was confirmed even in animals treated with FNP alone, including both the oral and the intraperitoneal application of the substance. The cardioprotective effects of FNP in animals previously treated with DOX were recognized to a certain extent, but were not fully confirmed at the ultrastructural level. Nevertheless, the myocardial morphology of DOX-treated animals improved after the admission of FNP. Irregular orientation of myofibrils, myofibrillar disruption, intracellular edema, and vacuolization were reduced, but not completely eliminated. Reduction of these cellular alterations was achieved if FNP was applied orally 6 h prior to DOX treatment in a dose of 18 mg/kg. However, numerous defects, including the inner mitochondrial membrane and the plasma membrane disruption of certain cells persisted. In FNP/DOX-treated animals, the presence of multinuclear cells with mitosis-like figures resembling metaphase or anaphase were observed, indicating that DOX and FNP could have a complex influence on the cell cycle of cardiomyocytes. Based on this experiment, further careful increase in dosage may be advised to enhance FNP-induced cardioprotection. These investigations should, however, always be combined with ultrastructural analysis. The FNP/DOX interaction is an excellent model for the investigation of cardiomyocyte cell death and cell cycle mechanisms. |
Databáze: | OpenAIRE |
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