Apoptosis: This term has been used to a mechanism of cell death that may affect single cells discrete in a population of healthy cells. It varies from necrosis and signifies a physiological process by which abnormal cells die and are eliminated.
Causes
Physiological
Ø The programmed destruction of cells during the embryogenesis include- implantation, organogenesis, metamorphosis, etc.
Ø Hormone dependent involution of tissues in the adult, e.g. endometrium, prostate.
Ø Cell detection in proliferating cell populations. e.g. crypt epithelia of intestine.
Ø Host cells are died that have served their useful purpose. e.g. Neutrophills in an acute inflammatory response.
Ø Elimination of potentially harmful self reactive lymphocytes.
Ø Cellular death by cytotoxic T-cells, a defence mechanism in contrast to viruses and tumors.
Pathological
Ø Cellular death produced by a variety of injurious stimuli which are able to create necrosis, but when given in low doses induce apoptosis. e.g. radiation, mild thermal injury.
Ø Cell injury in certain viral diseases, e.g. hepatitis.
Ø Atrophy in parenchymal organs after duct obstruction- occurs in pancreas, kidney.
Ø Cellular death in tumors, most frequently during regression but also in actively growing tumors.
Aging mechanism
As like age, there are also physiologic as well as structural alterations in almost all organ systems. Aging is effected in individuals by genetic factors, diet, social conditions and the occurrence of age-related disease such as arteriosclerosis diabetes and arthritis. However age induced alterations in cells which could represent the progressive accumulation over the years of sublethal injury or cell death are thought to be important components of aging.
The tabular form of cellular responses to injury is given below:
Nature and severity of injurious stimulus | Cellular responses |
Changed physiologic stimuli | Cellular adaptations |
Ø Increased response, increased trophic stimulus (e.g. growth factor, hormone) | Ø Hypertrophy,hyperplasia |
Ø Decreased nutrients, stimulation | Ø Atrophy |
Ø Prolonged irritation (physical or chemical) | Ø Metaplasia |
Decreased oxygen supply: chemical injury: microbial infection | Cell injury |
Ø self limited and acute | Ø Acute flexible injury |
Ø Severe as well as progressive (including DNA damage) | Ø permanent injury Cell death |
· Nacrosis | |
· Apoptosis | |
Ø Minor chronic injury | Ø Subcellular alteration in various organelles |
Metabolic alterations, genetic or acquired | Intracellular accumulation, calcifications |
Prolonged life span with cumulative sublethal injury |
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