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Mitochondria participate in programmed cell death. Indeed, a fundamental element of the "theory of aging" implicates the involvement of free radicals of mitochondrial origin. Oxidative stress contributes to the opening of the mitochondrial permeability transition (MPT) pore, which leads to mitochondrial depolarization, swelling and subsequent release of cytochrome c from the mitochondrial intermembrane space, resulting in apoptosis. The illustration shows induction of the MPT by reactive oxygen species (ROS) produced by laser photoexcitation. A confocal image of fluorescence in a tetramethylrhodamine methyl ester-(TMRM)-loaded rat cardiac myocytes shows the accumulation of TMRM inside mitochondria in proportion to the membrane potential, {Delta}{Psi}m (see upper image, above). Confocal line-scan imaging of {Delta}{Psi}m (i.e., TMRM fluorescence) of individual mitochondria over time is shown (left). The sudden loss of {Delta}{Psi}m in individual mitochondria at a discrete moment in time is due to induction of the MPT.
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