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The induction of apoptosis by daunorubicin and idarubicin in human trisomic and diabetic fibroblasts

In this study, we investigated apoptosis induced in human trisomic and diabetic fibroblasts by daunorubicin (DNR) and its derivative, idarubicin (IDA). The cells were incubated with DNR or IDA for 2 h and then cultured in a drug-free medium for a further 2–48 h. The apoptosis in the cultured cell li...

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Autores principales: Dragojew, Sylwia, Marczak, Agnieszka, Maszewski, Janusz, Ilnicki, Krzysztof, Jóźwiak, Zofia
Formato: Online Artículo Texto
Lenguaje:English
Publicado: SP Versita 2008
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6275653/
https://www.ncbi.nlm.nih.gov/pubmed/17965967
http://dx.doi.org/10.2478/s11658-007-0045-7
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author Dragojew, Sylwia
Marczak, Agnieszka
Maszewski, Janusz
Ilnicki, Krzysztof
Jóźwiak, Zofia
author_facet Dragojew, Sylwia
Marczak, Agnieszka
Maszewski, Janusz
Ilnicki, Krzysztof
Jóźwiak, Zofia
author_sort Dragojew, Sylwia
collection PubMed
description In this study, we investigated apoptosis induced in human trisomic and diabetic fibroblasts by daunorubicin (DNR) and its derivative, idarubicin (IDA). The cells were incubated with DNR or IDA for 2 h and then cultured in a drug-free medium for a further 2–48 h. The apoptosis in the cultured cell lines was assessed by biochemical analysis. We found that both drugs induced a timedependent loss of mitochondrial membrane potential, and a significant increase in intracellular calcium and caspase-3 activity. Mitochondrial polarization and changes in the level of intracellular calcium were observed during the first 2–6 h after drug treatment. Caspase-3 activation occurred in the late stages of the apoptotic pathway. Our findings also demonstrated that idarubicin was more cytotoxic and more effective than daunorubicin in inducing apoptosis in trisomic and diabetic fibroblasts.
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spelling pubmed-62756532018-12-10 The induction of apoptosis by daunorubicin and idarubicin in human trisomic and diabetic fibroblasts Dragojew, Sylwia Marczak, Agnieszka Maszewski, Janusz Ilnicki, Krzysztof Jóźwiak, Zofia Cell Mol Biol Lett Research Article In this study, we investigated apoptosis induced in human trisomic and diabetic fibroblasts by daunorubicin (DNR) and its derivative, idarubicin (IDA). The cells were incubated with DNR or IDA for 2 h and then cultured in a drug-free medium for a further 2–48 h. The apoptosis in the cultured cell lines was assessed by biochemical analysis. We found that both drugs induced a timedependent loss of mitochondrial membrane potential, and a significant increase in intracellular calcium and caspase-3 activity. Mitochondrial polarization and changes in the level of intracellular calcium were observed during the first 2–6 h after drug treatment. Caspase-3 activation occurred in the late stages of the apoptotic pathway. Our findings also demonstrated that idarubicin was more cytotoxic and more effective than daunorubicin in inducing apoptosis in trisomic and diabetic fibroblasts. SP Versita 2008-04-10 /pmc/articles/PMC6275653/ /pubmed/17965967 http://dx.doi.org/10.2478/s11658-007-0045-7 Text en © Versita 2007
spellingShingle Research Article
Dragojew, Sylwia
Marczak, Agnieszka
Maszewski, Janusz
Ilnicki, Krzysztof
Jóźwiak, Zofia
The induction of apoptosis by daunorubicin and idarubicin in human trisomic and diabetic fibroblasts
title The induction of apoptosis by daunorubicin and idarubicin in human trisomic and diabetic fibroblasts
title_full The induction of apoptosis by daunorubicin and idarubicin in human trisomic and diabetic fibroblasts
title_fullStr The induction of apoptosis by daunorubicin and idarubicin in human trisomic and diabetic fibroblasts
title_full_unstemmed The induction of apoptosis by daunorubicin and idarubicin in human trisomic and diabetic fibroblasts
title_short The induction of apoptosis by daunorubicin and idarubicin in human trisomic and diabetic fibroblasts
title_sort induction of apoptosis by daunorubicin and idarubicin in human trisomic and diabetic fibroblasts
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6275653/
https://www.ncbi.nlm.nih.gov/pubmed/17965967
http://dx.doi.org/10.2478/s11658-007-0045-7
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