Reactive oxygen species (ROS) and mitochondria play an important role in ap
optosis induction under both physiologic and pathologic conditions. Interes
tingly, mitochondria are both source and target of ROS. Cytochrome c releas
e from mitochondria, that triggers caspase activation, appears to be largel
y mediated by direct or indirect ROS action. On the other hand, ROS have al
so anti-apoptotic effects. This review focuses on the role of ROS in the re
gulation of apoptosis, especially in inflammatory cells.