Lecture 12 Flashcards
what can necrosis be initiated by (general)
cellular trauma, injury, or metabolic or environmental challenge
how can necrosis happen
- cell membranes rupture or become permeable
- reduction of production of ATP leads to loss of ability to maintain normal ionic differences across membranes
- fluid rushes into cell and ruptures
- intracellular proteolytic enzymes disassemble cellular components
what happens when content from injured cells are released into extracellular space
- they can damage adjacent healthy cells
- cytokines released lead to activation of macrophages and initiate inflammatory reaction
what are caspases
protease with cysteine at active site cleaving protein at aspartic site
what is the caspase cascade
aggregative of procaspases intimated activation of initiator caspases which then autophosphorylate and disassemble the cell
what happens to nuclear material and proteins after apoptosis
they are packaged into apoptotic bodies and taken up and recycled by healthy adjacent cells
what is the stimulus for extrinsic activation of apoptosis
cancerous cells, infected or obsolete cells
what is the pathway of death in extrinsic activation
Fas protein presents on external cell surface and killer lymphocyte binds with the fas ligand to form a complex with fas protein which gather intracellular adaptor proteins that aggregate procaspases
what inhibits procaspases from turning on when they’re not supposed to
inhibitor of apoptosis proteins (IAPs)
what is the stimulus for intrinsic activation of apoptosis
stressed or non nourished cells, intracellular damage, post radiation, DNA damage, oxidative stress
what is the pathway of death in intrinsic activation
mitochondria becomes leaky and cytochrome C leaks into cytoplasm where it binds to apaf-1 which binds to procaspases
how do you avoid apoptosis
decrease release of initial signal or increase synthesis of IAPs
