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Paclitaxel Induces Release of Cytochrome c from Mitochondria Isolated from Human Neuroblastoma Cells¹

UPRESA Centre National de la Recherche Scientifique 6032, Universite de la Mediterranée, Faculty of Pharmacy, 13005 Marseille, France [N. A., D. B., A. G., S. G., C. B.]; Department of Proteins, Bioenergetics, and Engineering, Centre National de la Recherche Scientifique, 13402 Marseille Cedex 20, France [G. B., D. L-M.]; Department of Pediatric Oncology, Children’s Hospital of La Timone,13005 Marseille, France [N. A.]; and Department of Molecular, Cellular, and Developmental Biology, University of California, Santa Barbara, California 93106-9610 [M. A. J.]

Paclitaxel is an antimicrotubule agent that induces mitotic block and apoptosis. We show for the first time that paclitaxel acts directly on mitochondria isolated from human cancer cells. In isolated yeast mitochondria, paclitaxel (15 µM) induced an 18% increase in the respiration rate, with no concomitant release of cytochrome c. In isolated neuroblastoma mitochondria, paclitaxel (10–100 µM) induced a 27–72% release of cytochrome c. Release was prevented by cyclosporin A, suggesting the involvement of the permeability transition pore. Doxorubicin did not induce cytochrome c release, whereas vinorelbine, another antimicrotubule agent, did. Thus, antimicrotubule agents can directly affect mitochondria to induce apoptosis.

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