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Similar to cell death. microbiology easy 2nd year ppt
cell death. microbiology easy 2nd year ppt
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- 2. Cell Cycle • Onlyfrom existing cells come new cells. • We are all decedents of the first cells on the planet. • A cell reproduces by duplicating its contents and then dividing into two • This cycle of events is known as the cell cycle Eukaryotic Cell Cycle
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- 4. Cell death • Thebody 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. • Two forms – Apoptosis - suicide - programmed cell death – Necrosis - killing - decay and destruction
- 5. Normal cell Small blebs Big blebs,no organelles Cellmembrane ruptures, organelles non functional Apinoptthoetic bbloebdsies, organelles functional, no inflammation DNA fragmentatio n, organ elles Small blebs necrosis apoptosis Inflammation of surrounding tissues
- 6. 1- Necrosis • Necrosisis the sum total of morphologic changes that follow cell death in a living tissue or organ • Dead cells usually show changes in both the cytolasm and in the nucleus. .
- 7. 1- Necrosis • Cytoplasmicchanges are: increases eosinohilia, glassy appearance, granular or vacuolated cytolasm, swollen mitochondria, may also show calcification • Nuclear changes: Karyolysis , Pyknosis and Karyorrhexis.
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- 9. Causes Necrosis may occurdue to external or internal factors: External factors may involve 1.Mechanical trauma (physical damage to the body that causes cellular breakdown) 2.Damage to blood vessels (which may disrupt blood supply to associated tissue), 3.Thermal effects (extremely high or low temperature) can result in necrosis due to the disruption of cells.
- 10. Causes Internal factors causingnecrosis include 1.Trophoneurotic disorders; injury and paralysis of nerve cells. 2.Pancreatic enzymes (lipases) are the major cause of fat necrosis. 3.necrosis programs in cells with immunological barriers (intestinal mucosa) may alleviate invasion of pathogens through surfaces affected by inflammation 4.Bacterial toxins; activated natural killer cells; and peritoneal macrophages. 5.necrosis programs in cells with immunological barriers (intestinal mucosa) may alleviate invasion of pathogens through surfaces affected by inflammation
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- 12. Mechanisms of Necrosis NecroticCell Death •Loss of metabolic functions •Loss of the integrity of the cell membranes •Cessation of the production of proteins and ATP. •Cells organelles swell and become nonfunctional.
- 13. Mechanisms of Necrosis 1.Depletion of ATP-leads to breakdown of the cell’s ion balance 2. Reduce oxygen level (hypoxia) 3. Oxidative stress - the presence of excess oxygen radicals
- 14. What are thetypes of necrosis? 1. Coagulation Necrosis 2. Liquefactive Necrosis 3. Fat Necrosis 4. Caseous Necrosis 5. Gangrenous Necrosis 6. Fibrinoid Necrosis
- 15. Necrosis types: 1.Coagulation Necrosis Seethis in infarcts in any tissue (except brain) •Due to loss of blood •Cell outlines are preserved and everything looks red.
- 16. Necrosis types 2.Liquefactive Necrosis •Seethis in infections in brain infarcts •Due to lots of neutrophils around releasing their toxic contents, “liquefying” the tissue. •tissue is liquidly and creamy yellow (pus) •lots of neutrophils and cell debris
- 17. Necrosis types: 3.Fat Necrosis: •fatnecrosis that in which the neutral fats in adipose tissue are split into fatty acids and glycerol, usually affecting the pancreas •shadowy outlines of dead fat cells
- 18. Necrosis types: 4.CASEOUS NECROSIS- LUNGS •cheesynecrosis that in which the tissue is soft, dry, and cottage cheese–like; most often seen in tuberculosis and syphilis.
- 19. Necrosis types: 5.Gangrenous Necrosis •See thiswhen an entire limb loses blood supply and dies •skin looks black and dead; underlying tissue is in varying stages of decomposition •initially there is coagulative necrosis from the loss of blood supply (this stage is called “dry gangrene”); if bacterial infection is superimposed, there is liquefactive necrosis (this stage is called “wet gangrene”).
- 20. Necrosis types 6.Fibrinoid necrosis •Seethis in immune reactions in vessels •Complexes of antigens and antibodies (immune complexes) combine with fibrin •changes too small to see grossly •vessel walls are thickened and pinkish-red (called “fibrinoid”
- 21. 2_ apoptosis programmed celldeath •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.
- 22. Apoptosi s programmed cell death •Form of cell death, in which a ‘suicide’ program is activated within the cell, leading to: • fragmentation of the DNA. • shrinkage of the cytoplasm. • membrane changes and cell death without lysis or damage to neighboring cells.
- 23. General characteristics of apoptosis •It is a normal phenomenon, occurring frequently in a multicellular organism. • a cell that undergoes apoptosis dies neatly, without damaging its neighbors. The cell shrinks and condenses. • There is no inflammation in apoptosis.
- 24. Importance of apoptosis 1_Programmed cell death is needed for proper normal development as mitosis is. Examples: – •The moldiness of the tadpole tail in frog . •The formation of the fingers and toes of the fetus requires the removal, by apoptosis. •The sloughing off of the endometrium at the start of menstruation.
- 25. Importance of apoptosis (cont..) •Example: Incomplete differentiation in two toes due to lack of apoptosis
- 26. Importance of apoptosis 2.Programmedcell 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).
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- 29. Biochemical features of apoptosis •DNAbreak down in apoptosis. •protein cleavage •phagocytic.
- 30. Mechanisms of apoptosis •Apoptosis occur in two phases: 1. Initiation phase: It happen when apoptotic enzymes are getting activated. 1. Execution phase: Activating enzymes are causing cell death.
- 31. Mechanisms of apoptosis •Initiation phase: 1. Extrinsic pathway. 2. Intrinsic pathway.
- 32. 1) Extrinsic pathway •Called death receptor pathway, mediated by: death receptors. • TNF family protein( tumor necrosis factor) .e.g. TNF R1, TNF fas. • Caspase are ( Cysteine- Aspartic acid) specific proteases that mediates the events that are associated with programmed cell death.
- 33. 1) Extrinsic pathway •Apoptosis initiated by extrinsic pathway. • In cytoplasmic side death receptor has death domains.
- 34. 1) Extrinsic pathway •Fas L( fas ligand) bind to fas receptor, and form cross link between three or more fas receptor then they can form binding site for adaptor molecule called death domain, which attract inactivated pro_ caspases and FADD( fas associated death domain).
- 35. 1) Extrinsic pathway •Caspases 8 start to cleave other pro_ caspases to result active form of caspases. • These caspases go to execution phase and causing apoptosis.
- 36. 2) Intrinsic pathway •Known as mitochondrial pathway. • Apoptosis occur due to increase permeability of mitochondria.
- 37. 2) Intrinsic pathway •In normal situation, • growth growth factor bind to receptor in plasma membrane formation of apoptotic which causing some anti_ .e.g. in protei n X Bcl2, Bcl mitochondria membrane. •Those will prevent leakage of pro_ apoptotic molecule.
- 39. 2) Intrinsic pathway •Radiation and other factors assist to remove these signal • Increasing resulting the leakage of pro_ permeability of mitochondria molecules from apoptotic mitochondria to cytoplasm. e.g. Bcl 2, and BclX via other type of pro_ apoptotic proteins such as Bak, and Bax.
- 40. 2) Intrinsic pathway •In cytosol, • Pro-apoptotic Factors Damage to the mitochondrial membrane increasing permeability Entry of Cytochrome C into the cytoplasm • Cytochrome c will bind to another molecule known as ApaF1 ( apoptosis activity factor 1) which activate caspases 9 resulting apoptosome .
- 41. 2) Intrinsic pathway •Apoptosome activates procaspase-9 to caspase-9 • Caspase-9 cleaves and activates pro_ caspase-3 and pro_ caspase-7. • This executioner caspases activate a cascade of proteolytic activity that leads to apoptosis.
- 42. 2) Intrinsic pathway •Other factor releasing form mitochondria is apoptosis inducing factor that neutralize anti_ apoptosis factor and promote apoptosis.
- 44. Execution phase • Itis mediated by caspase 3 and caspase 6 , recall caspase 8 and caspase 9(initiation caspases). • When it’s activated, they form sequence chain of reaction that can activate Caspase 3 and 6. • They break down cytoskeleton protein, and nuclear matrix protein that resulting breaking the nucleus.
- 45. Role in diseases •Too much apoptosis: Tissue atrophy. • Too little apoptosis: Cancer, Atherosclerosis.
- 46. APOPTOSIS & NECROSIS APOPTOSISNECROSIS NATURAL YES NO EFFECTS BENEFICIAL DETRIMENTAL Physiological or pathological Always pathological Single cells Sheets of cells Energy dependent Energy independent Cell shrinkage Cell swelling Membrane integrity maintained Membrane integrity lost
- 47. APOPTOSIS & NECROSIS APOPTOSISNECROSIS Role for mitochondria and cytochrome C No role for mitochondria No leak of lysosomal enzymes Leak of lysosomal enzymes Characteristic nuclear changes Nuclei lost Apoptotic bodies form Do not form DNA cleavage No DNA cleavage Activation of specific proteases No activation Regulatable process Not regulated Evolutionarily conserved Not conserved Dead cells ingested by neighboring cells Dead cells ingested by neutrophils and macrophages
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