Nuclear and cytoplasmic changes in the apoptotic cells is due to
(Caspases): (19, 189 Robbins 9th edition)Activation and Function of Caspases* The mitochondrial and death receptor pathway lead to the activation of the initiator caspases, caspase 9 and - 8, respectively. Active forms of these enzymes are produced and these cleave and thereby activate another series of caspases that are called the executioner caspases. These activated caspases cleave numerous targets culminating in activation of nucleases that degrade DNA and nucleoproteins. Caspases also degrade components of nuclear matrix and cytoskeleton, leading to fragmentation of cells.* Both extrinsic or intrinsic pathway result in activation of a proteolytic cascade of caspases that destroys the cell* Mitochondrial outer membrane permeabilization is regulated by the balance between pro-apoptotic (eg BAX, BAK) and anti-apoptotic molecules (BCL2, BCL-XL) BH-3 only molecules activate apoptosis by tilting the balance in favour of the pro-apoptosis molecules.* The role of BCL2 in protecting tumour cells from apoptosis* TP53 is an important gene that induces apoptosis in cells that are unable to repair DNA damages
Oxygen free radicals
Caspases
Complement fixation
ATP ases
Cellular Pathology