© 1999 by Oxford University Press
Journal of the National Cancer Institute, Vol. 91, No. 9, 743-745,
May 5, 1999
© 1999 Oxford University Press
EDITORIALS |
Arsenic Trioxide, a Novel Mitochondriotoxic Anticancer Agent?
Affiliations of authors: G. Kroemer, Centre National de la Recherche Scientifique (CNRS), EST1984, Villejuif, France; H. de Thé, CNRS, UPR9051, Laboratoire associé No. 11 Comité de Paris de la Ligue contre le Cancer, Laboratoire associé à l'Université de Paris VII, Hôpital St. Louis, Paris, France.
Correspondence to: Guido Kroemer, M.D., Ph.D., Centre National de la Recherche Scientifique, Unité Propre de Recherche 420, Génétique Moléculaire et Biologie du Développement, 19, rue Guy Môquet, BP8, 94801 Villejuif Cedex, France (e-mail: kroemer@infobiogen.fr).
During the last few years, it has become increasingly clear that
mitochondria play a major rate-limiting role in apoptosis
(1-3). In general terms, the apoptotic process can be
subdivided into three phases: the initiation phase, the
decision/effector phase, and the degradation phase. During the
heterogeneous initiation phase, which is essentially premitochondrial,
specific pro-apoptotic signal transduction pathways or nonspecific
damage pathways are activated. These pathways converge on the
mitochondria during the decision/effector phase, where they trigger
progressive permeabilization of mitochondrial membranes, mostly as a
result of the action of the permeability transition pore complex
(PTPC). Thus, the mitochondrion (or to be more precise, the PTPC, which
interacts with the Bcl-2/Bax complex) "decides" the cell's fate
and determines the point of no return of the process (4,5).
The morphologic and biochemical features of apoptosis become manifest
during the postmitochondrial degradation phase, in
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