“Where,O Death,Is Thy Sting?” A Brief Review of Apoptosis Biology

Apoptosis was a term introduced in 1972 to distinguish a mode of cell death with characteristic morphology and apparently regulated, endogenously driven mechanisms. The effector processes responsible for apoptosis are now mostly well known, involving activation of caspases and Bcl2 family members in response to a wide variety of physiological and injury-induced signals. The factors that lead of the decision to activate apoptosis as opposed to adaptive responses to such signals (e.g. autophagy, cycle arrest, protein synthesis shutoff) are less well understood, but the intranuclear Promyelocytic Leukaemia Body (PML body) may create a local microenvironment in which the audit of DNA damage may occur, informed by the extent of the damage, the adequacy of its repair and other aspects of cell status.     

Modification of mitochondria in cultivated hepatocytes as a function of the protein content of the medium]

Embryonic liver cells of chicken have been cultivated in medium more or less supplemented with serum. With a rich medium mitochondria become larger and often ramify. Their fundamental structure remains normal. It is only a hypertrophic condition correlated to an increase of mitochondrial material synthesis, limited to liver mitochondria.