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Week 13
Sources :
https://www.youtube.com/watch?v=1vaEVcMfa1E
https://www.youtube.com/watch?v=-vmtK-bAC5E
Cell Death
Introduction
• Necrosis( e.gtoxins, High temp ) uncontrolled –Pathological
process
• vs Apoptosis( Natural cell death;) –Suicide
Accumulated dead cells ----tumor; cells die too fast----herat
disease AIDS )
• Differences in structural changes between both processes
• Differences in Biochemical reaction ( Necrosis : passive
process doesn’t need energy-Random;Apoptosis active
process required energy –Organized manner
programmed cell death
(PCD)
1-Apoptosis involves cell shrinkage and blebbing
fragmentation of the nucleus, degradation of DNA to nucleosome‐ size
fragments and eventual phagocytises by other cells
Caspases-cells broken through apoptosis
which degrade poly‐ADPR polymerase (involved in DNA repair)and
cytoskeletal proteins required to maintain cell shape.
Activation of caspases
1-Extrinsic pathway : ( T-Lymphocytes )external signals, often via the
“death receptor” Fas (CD95)-receptor
2-Intrinsic internal DNA damage, A key step is the release of cytochrome
c from mitochondria leading to the activation of caspase 9
External
T-lymphocytes : surface ( fas ligand )
The target cell ( fas receptor )
When they bind they are stimulate ( FADD)
And after that it starts the self amplifying process
( caspase cascade-caspase activated each others )
Internal
In Mitochondrial membrane keep balance between they 2
proteins
1-Anti-apoptotic proteins (BCL-2 / BCL-x )
2-Pro-apoptotic proteins ( BAX / BAK )
Healthy cells : Anti-apoptotic proteins binds pro-apoptotic
proteins- block reaction
*
• If cell damaged ,
• BCL-2 And BCL-x blocked
• BAX And BAK free to punch a series of channels in mitochondria
membrane, allowing mitochondria substance such as Cytochrome
C leak to cytoplasm
• *Cytochrome C binds to Apache-1 proteins –create compound To
activates the caspase cascade
programmed cell death
(PCD)
Apoptosis plays a key role in
1-Growth
2-Immune surveillance
3-Neoplastic development
Unprogrammed cell death
2- Necrosis : is a form of cell injury which results
in the premature
Death of cell in living tissue by
autolysis.
Necrosis
• Necrosis is the death of body tissue. It occurs when too little blood
flows to the tissue. This can be from injury, radiation, or chemicals.
Necrosis cannot be reversed. When large areas of tissue die due to a
lack of blood supply, the condition is called gangrene.
Necrosis
Apoptosis
Loss of membrane integrity
No-loss of membrane integrity
(Blebbing occurs)
Cell membrane
Begins with swelling
Begins with cell And nucleus
shrinkage
Cell status and organelles
No vesicle formation
Complete cell lysis
Formation of apoptotic bodies
Vesicle formation
No response
There is a response
Inflammatory response
Causes
caused by factors external to the cell or tissue, such as infection, or
trauma which result in the unregulated digestion of cell components

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WEEK 12 2023 Apoptosis.pptx

  • 3. Introduction • Necrosis( e.gtoxins, High temp ) uncontrolled –Pathological process • vs Apoptosis( Natural cell death;) –Suicide Accumulated dead cells ----tumor; cells die too fast----herat disease AIDS ) • Differences in structural changes between both processes • Differences in Biochemical reaction ( Necrosis : passive process doesn’t need energy-Random;Apoptosis active process required energy –Organized manner
  • 4. programmed cell death (PCD) 1-Apoptosis involves cell shrinkage and blebbing fragmentation of the nucleus, degradation of DNA to nucleosome‐ size fragments and eventual phagocytises by other cells
  • 5. Caspases-cells broken through apoptosis which degrade poly‐ADPR polymerase (involved in DNA repair)and cytoskeletal proteins required to maintain cell shape. Activation of caspases 1-Extrinsic pathway : ( T-Lymphocytes )external signals, often via the “death receptor” Fas (CD95)-receptor 2-Intrinsic internal DNA damage, A key step is the release of cytochrome c from mitochondria leading to the activation of caspase 9
  • 6. External T-lymphocytes : surface ( fas ligand ) The target cell ( fas receptor ) When they bind they are stimulate ( FADD) And after that it starts the self amplifying process ( caspase cascade-caspase activated each others )
  • 7. Internal In Mitochondrial membrane keep balance between they 2 proteins 1-Anti-apoptotic proteins (BCL-2 / BCL-x ) 2-Pro-apoptotic proteins ( BAX / BAK ) Healthy cells : Anti-apoptotic proteins binds pro-apoptotic proteins- block reaction *
  • 8. • If cell damaged , • BCL-2 And BCL-x blocked • BAX And BAK free to punch a series of channels in mitochondria membrane, allowing mitochondria substance such as Cytochrome C leak to cytoplasm • *Cytochrome C binds to Apache-1 proteins –create compound To activates the caspase cascade
  • 10. Apoptosis plays a key role in 1-Growth 2-Immune surveillance 3-Neoplastic development
  • 11.
  • 12. Unprogrammed cell death 2- Necrosis : is a form of cell injury which results in the premature Death of cell in living tissue by autolysis.
  • 13. Necrosis • Necrosis is the death of body tissue. It occurs when too little blood flows to the tissue. This can be from injury, radiation, or chemicals. Necrosis cannot be reversed. When large areas of tissue die due to a lack of blood supply, the condition is called gangrene.
  • 14.
  • 15. Necrosis Apoptosis Loss of membrane integrity No-loss of membrane integrity (Blebbing occurs) Cell membrane Begins with swelling Begins with cell And nucleus shrinkage Cell status and organelles No vesicle formation Complete cell lysis Formation of apoptotic bodies Vesicle formation No response There is a response Inflammatory response
  • 16. Causes caused by factors external to the cell or tissue, such as infection, or trauma which result in the unregulated digestion of cell components