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UNIT -4
MECHANISM OF CELL INJURY
BY- JYOTI BALMIKI
MECHANISM OF CELL INJURY
Injury to cells may have many causes. In such case oxygen plays a central role in the cell injury. Mechanisms of cell injury
include-
 Ischemic and Hypoxic cell injury:
Cell membrane damage
• Mitochondrial damage
• Ribosome damage
• Nuclear damage
FREE RADICAL INDUCED CELL INJURY
Free radicals are chemical species that have a single unpaired
electron in outer orbit.
Free radicals initiate autocatalytic reaction.
It is mainly occur in reperfusion of the ischemic cell.
There are many more causes like chemical injury, cellular aging,
hyperoxia, killing of exogenious biological agents, destruction of
tumor cells, inflammatory damage, chemical injuries, ionization,
artherosclerogenesis.
There are some radicals, like superoxide radicals, hydroxyl ions,
peroxide ions, very destructive to cells which cause lipid
peroxidation, oxidation of protein, DNA damage, cytoskeleton
damage etc.
CELL MEMBRANE DAMAGE
Physical agents such as heat or radiation can damage a cell by literally cooking or coagulating their contents.
Impaired nutrient supply, such as lack of oxygen or glucose, or impaired production of adenosine triphosphate (ATP) may deprive the
cell of essential materials needed to survive.
MITOCHONDRIAL DAMAGE
Increases in cytosolic Calcium, coupled by an increase in inorganic phosphate and certain fatty acids.
High inorganic phosphate and fatty acids alone cannot damage the mitochondria but coupled with high Ca2+ are extremely
damaging to a cell.
Note that high Calcium alone can still damage mitochondria.
Leading to altered protein synthesis.
If hypoxia continues, intracellular protein synthesis decreases due to damage to ribosomes and polysomes.
Continue hypoxia causes cytoskeleton changes with loss of microvilli and formation of blebs on the surface of the
cell.
This swelling results in swelling at mitochondria and ER (endoplasmic reticulum).
NUCLEAR DAMAGE
The decrease in cellular ATP and increase in adenosine monophosphate (AMP) also stimulates the enzyme
phosphofructokinase glycolysis in order to maintain the cells energy source by generating the ATP from
glycogen.
This stage is reversible if oxygen is restored.
Unit -4 pathology.pptx

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Unit -4 pathology.pptx

  • 1. UNIT -4 MECHANISM OF CELL INJURY BY- JYOTI BALMIKI
  • 2. MECHANISM OF CELL INJURY Injury to cells may have many causes. In such case oxygen plays a central role in the cell injury. Mechanisms of cell injury include-  Ischemic and Hypoxic cell injury: Cell membrane damage • Mitochondrial damage • Ribosome damage • Nuclear damage
  • 3. FREE RADICAL INDUCED CELL INJURY Free radicals are chemical species that have a single unpaired electron in outer orbit. Free radicals initiate autocatalytic reaction. It is mainly occur in reperfusion of the ischemic cell. There are many more causes like chemical injury, cellular aging, hyperoxia, killing of exogenious biological agents, destruction of tumor cells, inflammatory damage, chemical injuries, ionization, artherosclerogenesis. There are some radicals, like superoxide radicals, hydroxyl ions, peroxide ions, very destructive to cells which cause lipid peroxidation, oxidation of protein, DNA damage, cytoskeleton damage etc.
  • 4.
  • 5. CELL MEMBRANE DAMAGE Physical agents such as heat or radiation can damage a cell by literally cooking or coagulating their contents. Impaired nutrient supply, such as lack of oxygen or glucose, or impaired production of adenosine triphosphate (ATP) may deprive the cell of essential materials needed to survive.
  • 6.
  • 7. MITOCHONDRIAL DAMAGE Increases in cytosolic Calcium, coupled by an increase in inorganic phosphate and certain fatty acids. High inorganic phosphate and fatty acids alone cannot damage the mitochondria but coupled with high Ca2+ are extremely damaging to a cell. Note that high Calcium alone can still damage mitochondria.
  • 8.
  • 9. Leading to altered protein synthesis. If hypoxia continues, intracellular protein synthesis decreases due to damage to ribosomes and polysomes. Continue hypoxia causes cytoskeleton changes with loss of microvilli and formation of blebs on the surface of the cell. This swelling results in swelling at mitochondria and ER (endoplasmic reticulum).
  • 10. NUCLEAR DAMAGE The decrease in cellular ATP and increase in adenosine monophosphate (AMP) also stimulates the enzyme phosphofructokinase glycolysis in order to maintain the cells energy source by generating the ATP from glycogen. This stage is reversible if oxygen is restored.