Oxidative stress and apoptosis Krishnaswamy Kannan, Sushil K Jain  Pathophysiology  Volume 7, Issue 3, Pages 153-163 (September 2000) DOI: 10.1016/S0928-4680(00)00053-5

Fig. 1 Schematic model of mammalian cell death pathway. Death signal may be delivered at the cell surface by direct ligand-receptor interaction. This followed by clustering of death receptors and activation of caspase-8. Alternatively, cytotoxic drugs, ionizing radiation may directly activate caspase-9, otherwise a later event. Mitochondria plays a central role in apoptosis by releasing apoptogenic factors and proteases into the cytosol. A major checkpoint in this pathway is the ratio between pro-apoptotic (Bax) to anti-apoptotic (Bcl-2) members. Miitochondrial dysfunction includes PT, change in mitochondrial membrane potential, production of ROS, release of cytochrome C, AIPF-1 and caspases-2, -3, and -9 into the cytosol, where they form multimeric complexes. This activates downstream caspases and degradation of death substrates in the nucleus, which ultimately leads to cell death. Pathophysiology 2000 7, 153-163DOI: (10.1016/S0928-4680(00)00053-5)