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Vol. 56, Issue 5, 867-874, November 1999

Implication of Radical Oxygen Species in Ceramide Generation, c-Jun N-Terminal Kinase Activation and Apoptosis Induced by Daunorubicin

Véronique Mansat-De Mas, Christine Bezombes, Anne Quillet-Mary, Ali Bettaïeb, Aurélie De Thonel D'orgeix, Guy Laurent, and Jean-Pierre Jaffrézou

Institut National de la Sante et de la Recherche Medicale E9910, Institut Claudius Régaud (V.M.D., C.B., A.Q.M., A.B., G.L., J.P.J.), and Service d'Hématologie, Centre Hospitalier Universitaire Purpan (G.L.), Toulouse, France

Anthracyclines such as daunorubicin (DNR) generate radical oxygen species (ROS), which account, at least in part, for their cytotoxic effect. We observed that early ceramide generation (within 6-10 min) through neutral sphingomyelinase stimulation was inhibitable by the antioxidants N-acetylcysteine and pyrrolidine dithiocarbamate, which led to a decrease in apoptosis (>95% decrease in DNA fragmentation after 6 h). Furthermore, we observed that DNR triggers the c-Jun N-terminal kinase (JNK) and the transcription factor activated protein-1 through an antioxidant-inhibitable mechanism. Treatment of U937 cells with cell-permeant ceramides induced both an increase in ROS generation and JNK activation, and apoptosis, all of which were antioxidant-sensitive. In conclusion, DNR-triggered apoptosis implicates a ceramide-mediated, ROS-dependent JNK and activated protein-1 activation.

Copyright © 1999 by The American Society for Pharmacology and Experimental Therapeutics


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