Showing posts with label Apoptosis. Show all posts
Showing posts with label Apoptosis. Show all posts

Monday, July 13, 2015

What is diffenece bteween Necrosis and Apoptosis

Give pathogenesis of Apoptosis.

Apoptosis result from the activation of enzymes called caspases. Like many proteases, casepases exist as inactive proenzymes or zymogens and must undergo enzymatic cleavage to become active.
The process of apoptosis may be divided into an Initiation phase during which some caspases become catalytically active and an execution phase during which other caspases trigger the degradation of critical cellular components. The activation of caspases depends on a finely tuned balance between production of pro-apoptotic and anti-apoptotic proteins.
Two distinct pathways converge on caspase activation:
A. The mitochondrial pathway
B. The death receptor pathway

The mitochondrial pathway or the intrinsic pathway is the major mechanism of apoptosis in all mammalian cells. It results from increased permeability of the mitochondrial outer membrane with consequent release of death inducing.

Friday, March 27, 2015

What do you mean by Apoptosis? What are the causes of Apoptosis?

Apoptosis:

Apoptosis is a pathway of cell death that is induced by a tightly regulated suicide program in which cells
destined to die activate intrinsic enzymes that degrade the cells’ own nuclear DNA and nuclear and cytoplasmic proteins.

Causes of Apoptosis:

Apoptosis occurs normally both during development and throughout adulthood, and serves to remove unwanted, aged, or potentially harmful cells. It is also a pathologic event when diseased cells become damaged beyond repair and are eliminated.

Apoptosis in Physiologic Situations:

  • The destruction of cells during embryogenesis, including implantation, organogenesis, developmental involution, and metamorphosis.
  • Involution of hormone-dependent tissues upon hormone withdrawal, such as endometrial cell breakdown during the menstrual cycle, ovarian follicular atresia in menopause, the regression of the lactating breast after weaning, and prostatic atrophy after castration.
  • Cell loss in proliferating cell populations, such as immature lymphocytes in the bone marrow and thymus and B lymphocytes in germinal centers that fail to express useful antigen receptors.
  • Elimination of potentially harmful self-reactive lymphocytes, either before or after they have completed their maturation, so as to prevent reactions against one’s own tissues.
  • Death of host cells that have served their useful purpose, such as neutrophils in an acute inflammatory response, and lymphocytes at the end of an immune response.

Apoptosis in Pathologic Conditions:

  • DNA damage. Radiation, cytotoxic anticancer drugs, and hypoxia can damage DNA, either directly or via production of free radicals.
  • Accumulation of misfolded proteins.
  • Cell death in certain infections, particularly viral infections, in which loss of infected cells is largely due to apoptosis that may be induced by the virus (as in adenovirus and HIV infections) or by the host immune response (as in viral hepatitis).
  • Pathologic atrophy in parenchymal organs after duct obstruction, such as occurs in the pancreas, parotid gland, and kidney.