The mitochondria in cerebellar granule cells

Apoptosis -- the programmed cell death -- is a complicated process. The activity of many genes influences a cell's likelihood of activating its self-destruction program. Once "the decision" is taken, the apoptotic program, in the induction phase, requires the coordinated activation and execution of multiple events. They constitute a dedicated apoptotic signalling pathway converging into the common events of the execution phase. Oxidative stress has often been evoked as a mediator of this intracellular apoptotic signalling. Within a certain concentration range, reactive oxygen species (ROS) can induce stress response of the cells by altering expression of respiratory genes to uphold the energy metabolism to rescue the cell. However, ROS may both cause a wide spectrum of oxidative damage to various cellular components which result in cell death and elicit apoptosis by induction of release from mitochondria of apoptogenic factors including cytochrome c. A major role in apoptosis is also played by the antioxidant and the proteolytic cell systems. Mitochondria play a pivotal role in apoptosis being recently emerged as a convergence centre for life and death signals. Here we discuss how ROS act to regulate apoptosis in a coordinated manner and how the released cytochrome c participates to apoptosis, being able to act as an antioxidant itself, as well as responsible of caspase activation, which play a prominent role in the destructive phase of apoptosis. The role of the adenine nucleotide translocator will be also reported as a responsible for ATP export outside mitochondria and as a component of the mitochondrial permeability transition pore. Primary rat cerebellar granule cell culture will be considered as a model cell system and will be investigated en route to apoptosis.