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Mitochondrial reactive oxygen species and apoptosis
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Edité par CCSD -
International audience. Programmed cell death (PCD) serves as a major mechanism for the precise regulation of cellnumbers, and as a defense mechanism to remove unwanted and potentially dangerous cells. Despitethe striking heterogeneity of cell death induction pathways, the execution of the death program isoften associated with characteristic morphological and biochemical changes termed apoptosis.The central components of the intrinsic apoptotic pathway involve specific proteases (i.e.caspases) and mitochondria (Nunez et al., 1998; Raff, 1998). Although for a long time the absenceof mitochondrial changes was considered as a hallmark of apoptosis, mitochondria appear today asthe central executioner of programmed cell death. This crucial position of mitochondria inprogrammed cell death control is not due to a simple loss of function (deficit in energy supplying),but rather to an active process in the regulation of effector mechanisms. This role is reinforced bythe observation that mitochondria contribute to PCD signaling via the production of reactive oxygenspecies, as shown in TNF-α or ceramide-induced cell death during which increased mitochondrialROS production appears as an early event of the induction phase. Recent other reviews cover theabundant literature dealing with the role of mitochondrion in cell death (Bernardi et al., 1998;Bernardi et al., 1999; Mignotte and Kroemer, 1999; Mignotte and Vayssière, 1998; Mignotte andVayssière, 1999; Reed et al., 1998; Susin et al., 1998). In this chapter, we examine on the one handthe data concerning the mitochondrial proteins involved in PCD, and on the other hand the role ofreactive oxygen species (ROS) in mitochondrial features of apoptosis.
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