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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Detalles Bibliográficos
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
Descripción
Sumario: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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