Apoptosis is an “intricate, programmed pathway of cell death”, which is considered to be a more natural form of cell death as compared to necrosis. In apoptosis, the following steps are seen:
Cell shrinkage.
Condensation of nucleus contents.
DNA fragmentation.
In contrast to apoptosis, cell death seen with injury to the cell (necrosis) includes swelling and rupture of the cell wall with spreading of the cell’s contents into the space outside the cell. This results in extensive inflammation.
Trigger agents for apoptosis can be external. There are receptors on the cell surface that are called “death receptors.” A chemical produced externally called Tumor Necrosis Factor (TNF) binds on the surface of the cell receptor sites and stimulates internal enzymes called caspases. There is an internal pathway for apoptosis that centers in the mitochondria.
Apoptosis is valuable in removing dysfunctional and mutated cells from the body. Necrosis type cell death results in excessive inflammation when the cell contents, such as enzymes, are suddenly released into the extracellular space. The dysfunctional and mutant cells consumed by apoptosis would include cancerous cells and autoimmune cells.
Phagocytes are white cells that clean up the debris from cell death. As cells die, phosphatidylserine (PS) turns from the inner cell membrane to the outer cell space. Phagocytes recognize the PS and are stimulated to start the cleanup process of phagocytosis, which includes surrounding the cell debris and digesting it. As the PS goes outside the cell, sphingomyelin goes in and is consumed within the cell.
CONCLUSION: The goal of apoptosis, an orderly cell death, is to remove dysfunctional and mutant cells in a manner to minimize inflammation and maintain stability of the body as a whole.
NOTE: Phosphatidylserine is a phospholipid that is found on the inside of cell walls. Sphingomyelin is a phospholipid that is, normally, found in the outside of cell walls.
Read about the effect of Rhodiola rosea on apoptosis.
PMID: 16509786.
Summary #136.
