CELL INJURY

Mechanism of injury:

4 important events are:
  • membrane damage
  • mitochondrion damage and depletion of ATP
  • Influx of calcium
  • Accumulation of oxygen-derived free radicals
Many metabolic activity will stop without ATP. Membrane damage not only refer to the plasma membrane but also to those organelles membrane, especially mitochondria, lysosome and endoplasmic reticulum. All of them are bilayer lipid membrane. If the intact of membrane is broken, mitochondria will reduce the production of ATP for oxidative phosphorylation being damaged, often is the earliest event. Damaged RER slow down the rate of protein synthesis for detachment of ingredient from ER. Later a lot of calcium release from mitochondria and endoplasmic reticulum (both are intracellular calcium store), resulting in increase of cytosol calcium concentration, which is fatal to cell. Meanwhile, The membrane of lysosome breaks down, various hydrolases leak in the cytoplasm to digest the protein, lipid and DNA. The cell will die.
At beginning of injury, before energy exhausted, the lysosome will be active, engulf exogenous particles (heterophagy and endogenous particles, such as degrading protein and senescent organelles—-autophagy,  we have known that lipofuscin is a residum of autophagic vacuole.   Note all work be done inside the lysosome. The membrane keep other normal components in cell far from hydrolyses in the lysosome.
When the injury is severe and energy exhaust the permeability of lysosome membrane increase, various hydrolases will release out to degrade the components of protein and lipids in cytoplasm or on cell membrane. At last cell is broken.
https://www.hanxinclinic.com/index.php/2019/12/06/cell-injury-2/

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