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cell death by rasheed.pptx

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cell death by rasheed.pptx

  1. 1. Cell death ABDUL RASHEED EBRAHIM 1
  2. 2. Cell cycle 2 New cells are formed from the existing cell The cell is produced by duplicating the existed one and then they will divide in to two This event is called as cell cycle
  3. 3. Cell death The body is very good at maintaining a constant number of cells so there has to exist mechanisms for ensuring other cells in the body are removed when appropriate Cell death happens in two forms ◦ Apoptosis – suicide – programmed cell death ◦ Necrosis – killing – decay and destruction 3
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  5. 5. Necrosis Necrosis is the death of body tissue. It occurs when too little blood flows to the tissue. This can be formed by injury, radiation, or chemicals. Necrosis cannot be reversible These are dead cells shows changes in both cytoplasm and in the nucleus 5
  6. 6. Nuclear and cytoplasm 6 Cytoplasmic changes Nuclear changes Increases eosinophilia, glassy appearace granular or vacuolated cytoplasm, swellen mitochondria may also show calcification Karyolysis - complete dissolution of chromatins Karyorrhexis – chromatin is distributed irregularly Pyknosis – irreversible condensation of chromatins
  7. 7. Factors 7 NECROSIS MAY OCCUR DUE TO EXTERNAL AND INTERNAL FACTORS EXTERNAL FACTORS MAY INVOLVED MECHANICAL TRAUMA ( PHYSICAL DAMAGE TO THE BODY THAT CAUSES CELLULAR BREAK DOWN) DAMAGE TO BLOOD VESSELS (WHICH MAY DISRUPT BLOOD SUPPLY TO ASSOCIATED TISSUE) THERMAL EFFECT (EXTREMELY HIGH OR LOW TEMPERATURE CAN RESULT IN NECROSIS DUE TO DISRUPTION OF CELLS
  8. 8. Causes Internal factors causing necrosis includes 1. Trophoneurotic disorders - injury and paralysis of nerve cells 2. Pancreatic enzyme – are the major cause for the fat necrosis (lipases) 3. Immunological barriers – invasion of pathogen through surface affected by inflammation (intestinal mucosa) 4. Bacterial toxins – activated natural killer cells and peritoneal macrophages 5. Toxins and pathogens – may cause necrosis toxins such as venom may inhibit enzymes and cause cell death 8
  9. 9. Necrotic cell death LOSS OF METABOLIC FUCTION LOSS OF INTEGRITY OF THE CELL MEMBRANES CESSATION OF THE PRODUCTION OF PROTEIN CELL ORGANELLS SWELL AND BECOMES NON-FUNCTIONAL 9
  10. 10. Mechanisms of necrosis Depletion of ATP  leads to breakdown of the cells ion balance Reduce oxygen level (hypoxia) Oxidative stress  the presence of the excess oxygen radicals 10
  11. 11. Types of necrosis 1. Coagulation Necrosis 2. Liquefactive necrosis 3. Fat necrosis 4. Caseous necrosis 5. Gangrenous necrosis 6. Fibrinoid necrosis 11
  12. 12. Coagulation necrosis This types necrosis is seen in every tissues except brain They occurs due to the loss of blood Cell outlines are preserved and everything looks red 12
  13. 13. Liquefaction necrosis 13 This type of necrosis occurs as infection in brain infarcts Due to lots of neutrophiles around releasing their toxic contents “liquefying” the tissue Tissue is liquidly and creamy yellow (pus) Lots of neutrophils and cell debris
  14. 14. Fat necrosis Fat necrosis that in which the neutral fats in adipose tissue are split into fatty acids and glycerol usually affecting the pancreas Shadowy outline of dead fat cells 14
  15. 15. Caseous necrosis (lungs) Cheesy necrosis that in which the tissues is soft dry and cottage cheese-like :most ofte seen in tuberculosis and syphilis 15
  16. 16. Gangrenous necrosis See this when an entire limb loses blood supply and dies Skin looks black and dead:underlying tissues is in varying stages of decomposition Dry gangrene Initially there is coagulative necrosis from the loss of blood supply wet gangrene If bacterial infection is superimposed there is liquefactive necrosis 16
  17. 17. Fibrinoid necrosis Fibrinoid necrosis is a specific pattern of irreversible, uncontrolled cell death that occurs when antigen-antibody complexes are deposited in the walls of blood vessels along with fibrin  see this in immune reactions in vessels Complexes of antigen and antibodies It appears as too small and visible grossly Vessel walls are thickened and pinkish red  fibrinoid 17
  18. 18. Apoptosis Programmed cell death In human body cells were produced every second by mitosis there is a similar number die by apoptosis Between 50-70 billion cells die each day in adult Between 20-30 billion cells die each day in child 18
  19. 19. Programmed cell death It is a form of cell death in which a suicide program is activated within cells Which leads to Fragmentation of the DNA Shrinkage of the cytoplasm Membrane changes and cell death without lysis or damage to neighboring cells 19
  20. 20. Characteristics of apoptosis It is a normal phenomenon occurring frequently in a multicellular organism  A cell that undergoes apoptosis dies neatly without damaging its neighbour cells The cell will shrink and then condensed There will be no inflammation in apoptosis 20
  21. 21. Importance of apoptosis Programmed cell death is needed to destroy cells that represent a threat to the integrity of the organism Examples : Cells infected with viruses Cells with DNA damage Cancer cells (uncontrolled proliferated cells) 21
  22. 22. Biochemical feature of apoptosis DNA break down in apoptosis Protein cleavage Phagocytic 22
  23. 23. Mechanisms of apoptosis Apoptosis occurs in two phases : 1. Initiation phase: It happens when apoptotic enzymes are getting activated 2. Executive phase: activating enzymes are cause cell death Initiation phase : 1. Extrinsic pathway 2. Intrinsic pathway 23
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  25. 25. Extrinstic pathway  It is called as death receptor pathways  mediated by death receptor Caspase  are (cysteine – aspartic acid) specific proteases that mediates the events that are associated with programmed cell death 25
  26. 26. Executive phase it is mediated by caspase 3 and caspase 6 When it is activated they form sequence chain of reaction than can activates caspase 3 and 6 They break down cytoskeleton protein and neuclear matrix that result in the breaking of the nucleus 26
  27. 27. Difference in Necrosis & Apoptosis 27
  28. 28. Autophagy •Physiological conditions Aging Exercise Pathological Various disease cancer 28
  29. 29. Basic concept in mechanism Cellular stress  activates autophagy pathway 29 Phagophore formation • Isolation membrane • Derived from endoplasmic recticulum plasma membrane or mitochondria Autophagos ome • Formation of vesicles autophago lysosome • Fusion with lysosome
  30. 30. mechanism Autophagy related genes  which encodes protein called ATG protein  ATG proteins  needed for the formation of autophagosomes Depletion of growth factors activates  This ULK1 complex is called as initiation complex so this complex initiates the process of autophagy This forms preautophagosomal structure 30 ATG101 ATG13 ULK1
  31. 31. Mechanism 31 ATG14L VPS15 BECLIN 1 VPS34 That ULK1 complex activates  This complex is called as PI3K complex This stage is called as nucleation This activation of PI3K complex results in nucleation and formation of phagophore Phagosome formation
  32. 32. Elongation and maturation  This has to elongate and fuse to form Autophagosome For that they need a set of proteins called as ubiquitin like conjugation system The function of ubiquitin is identifying proteins to be degraded by the proteasome, but ubiquitination can play a role in other processes such as endocytosis and other forms of protein trafficking, transcription and transcription factor regulation, cell signaling, histone modification, and DNA repair. Ubiquitin like system covalently links lipid in phosphatidylethanolamine to the microtubule-associated protein light chain 3 (LC3) results in elongation and the fusion to form autophagosome During the process of autophagosome the cellular content will be trapped inside autophagosome 32
  33. 33. Degradation Lysosome comes near autophagosome and then fuses to form autophagolysosome Lysosomal contents enters into autophagosome and degradation of cells happens 33
  34. 34. Benefits of autophagy Its is a survival mechanism under stressful conditions It maintains the integrity of cells by recycling essential metabolites and clearing intracellular debris Intracellular debris occurs in  aging , under stress and in diseased state When such cell unable to cope the cell which is already in autophagy so autophagy itself trigger death 34
  35. 35. Roles of autophagy IN CANCER : In cancer cells, autophagy suppresses tumorigenesis by inhibiting cancer-cell survival and inducing cell death, but it also facilitates tumorigenesis by promoting cancer-cell proliferation and tumor growth .the mechanism of the autophagic process is controlled by a series of proteins 35
  36. 36. ROLES OF AUTOPHAGY ROLE OF AUTOPHAGY IN NEURODEGENARATIVE DISEASE  Increasing evidence suggests that dysregulation of autophagy results in the accumulation of abnormal proteins and/or damaged organelles, which is commonly observed in neurodegenerative diseases, such as Alzheimer, Huntington's, and Parkinson's diseases (Banerjee et al 36
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