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Int. J. Mol. Sci. 2014, 15(12), 22960-22977; doi:10.3390/ijms151222960

Modulation of Induced Cytotoxicity of Doxorubicin by Using Apoferritin and Liposomal Cages

1
Department of Pathological Physiology, Faculty of Medicine, Masaryk University, Kamenice 5, CZ-62500 Brno, Czech Republic
2
Central European Institute of Technology, Brno University of Technology, Technicka 3058/10, CZ-61600 Brno, Czech Republic
3
Department of Physiology, Faculty of Medicine, Masaryk University, Kamenice 5, CZ-62500 Brno, Czech Republic
4
Department of Chemistry and Biochemistry, Mendel University in Brno, Zemedelska 1, CZ-61300 Brno, Czech Republic
5
Department of Experimental Biology, Faculty of Science, Masaryk University, Kamenice 5, CZ-62500 Brno, Czech Republic
6
Department of Biochemistry, Faculty of Science, Charles University, Albertov 2030, CZ-12840 Prague 2, Czech Republic
*
Author to whom correspondence should be addressed.
Received: 3 September 2014 / Revised: 6 November 2014 / Accepted: 1 December 2014 / Published: 11 December 2014
(This article belongs to the Special Issue Bioactive Nanoparticles 2014)
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Abstract

Doxorubicin is an effective chemotherapeutic drug, however, its toxicity is a significant limitation in therapy. Encapsulation of doxorubicin inside liposomes or ferritin cages decreases cardiotoxicity while maintaining anticancer potency. We synthesized novel apoferritin- and liposome-encapsulated forms of doxorubicin (“Apodox” and “lip-8-dox”) and compared its toxicity with doxorubicin and Myocet on prostate cell lines. Three different prostatic cell lines PNT1A, 22Rv1, and LNCaP were chosen. The toxicity of the modified doxorubicin forms was compared to conventional doxorubicin using the MTT assay, real-time cell impedance-based cell growth method (RTCA), and flow cytometry. The efficiency of doxorubicin entrapment was 56% in apoferritin cages and 42% in the liposome carrier. The accuracy of the RTCA system was verified by flow-cytometric analysis of cell viability. The doxorubicin half maximal inhibition concentrations (IC50) were determined as 170.5, 234.0, and 169.0 nM for PNT1A, 22Rv1, and LNCaP, respectively by RTCA. Lip8-dox is less toxic on the non-tumor cell line PNT1A compared to doxorubicin, while still maintaining the toxicity to tumorous cell lines similar to doxorubicin or epirubicin (IC50 = 2076.7 nM for PNT1A vs. 935.3 and 729.0 nM for 22Rv1 and LNCaP). Apodox IC50 was determined as follows: 603.1, 1344.2, and 931.2 nM for PNT1A, 22Rv1, and LNCaP. View Full-Text
Keywords: doxorubicin; liposome; apoferritin; cancer; cardiotoxicity; modification; encapsulation doxorubicin; liposome; apoferritin; cancer; cardiotoxicity; modification; encapsulation
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This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. (CC BY 4.0).

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Gumulec, J.; Fojtu, M.; Raudenska, M.; Sztalmachova, M.; Skotakova, A.; Vlachova, J.; Skalickova, S.; Nejdl, L.; Kopel, P.; Knopfova, L.; Adam, V.; Kizek, R.; Stiborova, M.; Babula, P.; Masarik, M. Modulation of Induced Cytotoxicity of Doxorubicin by Using Apoferritin and Liposomal Cages. Int. J. Mol. Sci. 2014, 15, 22960-22977.

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