Implication of mitochondria-derived ROS and cardiolipin peroxidation in N-(4-hydroxyphenyl)retinamide-induced apoptosis

We have studied the effect of N-(4-hydroxyphenyl)retinamide on either malignant human leukaemia cells or normal cells and investigated its mechanism of action. We demonstrate that 4HPR induces reactive oxygen species increase on mitochondria at a target between mitochondrial respiratory chain comple...

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Autores principales: Asumendi, A, Morales, M C, Alvarez, A, Aréchaga, J, Pérez-Yarza, G
Formato: Texto
Lenguaje:English
Publicado: Nature Publishing Group 2002
Materias:
Experimental Therapeutics
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2375439/
https://www.ncbi.nlm.nih.gov/pubmed/12085192
http://dx.doi.org/10.1038/sj.bjc.6600356
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author Asumendi, A
Morales, M C
Alvarez, A
Aréchaga, J
Pérez-Yarza, G
author_facet Asumendi, A
Morales, M C
Alvarez, A
Aréchaga, J
Pérez-Yarza, G
author_sort Asumendi, A
collection PubMed
description We have studied the effect of N-(4-hydroxyphenyl)retinamide on either malignant human leukaemia cells or normal cells and investigated its mechanism of action. We demonstrate that 4HPR induces reactive oxygen species increase on mitochondria at a target between mitochondrial respiratory chain complex I and II. Such oxidative stress causes cardiolipin peroxidation which in turn allows cytochrome c release to cytosol, caspase-3 activation and therefore apoptotic consumption. Moreover, this apoptotic pathway seems to be bcl-2/bax independent and count only on malignant cells but not normal nor activated lymphocytes. British Journal of Cancer (2002) 86, 1951–1956. doi:10.1038/sj.bjc.6600356 www.bjcancer.com © 2002 Cancer Research UK
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spelling pubmed-23754392009-09-10 Implication of mitochondria-derived ROS and cardiolipin peroxidation in N-(4-hydroxyphenyl)retinamide-induced apoptosis Asumendi, A Morales, M C Alvarez, A Aréchaga, J Pérez-Yarza, G Br J Cancer Experimental Therapeutics We have studied the effect of N-(4-hydroxyphenyl)retinamide on either malignant human leukaemia cells or normal cells and investigated its mechanism of action. We demonstrate that 4HPR induces reactive oxygen species increase on mitochondria at a target between mitochondrial respiratory chain complex I and II. Such oxidative stress causes cardiolipin peroxidation which in turn allows cytochrome c release to cytosol, caspase-3 activation and therefore apoptotic consumption. Moreover, this apoptotic pathway seems to be bcl-2/bax independent and count only on malignant cells but not normal nor activated lymphocytes. British Journal of Cancer (2002) 86, 1951–1956. doi:10.1038/sj.bjc.6600356 www.bjcancer.com © 2002 Cancer Research UK Nature Publishing Group 2002-06-17 /pmc/articles/PMC2375439/ /pubmed/12085192 http://dx.doi.org/10.1038/sj.bjc.6600356 Text en Copyright © 2002 Cancer Research UK https://creativecommons.org/licenses/by/4.0/This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material.If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit https://creativecommons.org/licenses/by/4.0/.
spellingShingle Experimental Therapeutics
Asumendi, A
Morales, M C
Alvarez, A
Aréchaga, J
Pérez-Yarza, G
Implication of mitochondria-derived ROS and cardiolipin peroxidation in N-(4-hydroxyphenyl)retinamide-induced apoptosis
title Implication of mitochondria-derived ROS and cardiolipin peroxidation in N-(4-hydroxyphenyl)retinamide-induced apoptosis
title_full Implication of mitochondria-derived ROS and cardiolipin peroxidation in N-(4-hydroxyphenyl)retinamide-induced apoptosis
title_fullStr Implication of mitochondria-derived ROS and cardiolipin peroxidation in N-(4-hydroxyphenyl)retinamide-induced apoptosis
title_full_unstemmed Implication of mitochondria-derived ROS and cardiolipin peroxidation in N-(4-hydroxyphenyl)retinamide-induced apoptosis
title_short Implication of mitochondria-derived ROS and cardiolipin peroxidation in N-(4-hydroxyphenyl)retinamide-induced apoptosis
title_sort implication of mitochondria-derived ros and cardiolipin peroxidation in n-(4-hydroxyphenyl)retinamide-induced apoptosis
topic Experimental Therapeutics
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2375439/
https://www.ncbi.nlm.nih.gov/pubmed/12085192
http://dx.doi.org/10.1038/sj.bjc.6600356
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