Amongst other causes, this can be due to physical, chemical, infectious, biological, nutritional or immunological factors.
[2] Cell death is relative to both the length of exposure to a harmful stimulus and the severity of the damage caused.
On microscopic examination, small clear vacuoles may be seen within the cytoplasm; these represent distended and pinched-off segments of the endoplasmic reticulum.
In the liver, the enlargement of hepatocytes due to fatty change may compress adjacent bile canaliculi, leading to cholestasis.
Necrosis is characterised by cytoplasmic swelling, irreversible damage to the plasma membrane, and organelle breakdown leading to cell death.
[10] Cytosolic components that leak through the damaged plasma membrane into the extracellular space can incur an inflammatory response.
It is an energy-dependent process mediated by proteolytic enzymes called caspases, which trigger cell death through the cleaving of specific proteins in the cytoplasm and nucleus.
[14] There is some evidence that certain symptoms of "apoptosis" such as endonuclease activation can be spuriously induced without engaging a genetic cascade.
It is also becoming clear that mitosis and apoptosis are toggled or linked in some way and that the balance achieved depends on signals received from appropriate growth or survival factors.
The motto of the repair process is to fill a gap caused by the damaged cells to regain structural continuity.
[16] ATP (adenosine triphosphate) depletion is a common biological alteration that occurs with cellular injury.
Whereas DNA damages are abnormal chemical and structural alterations, mutations ordinarily involve the normal four bases in new arrangements.
In multicellular organisms, cell death in response to DNA damage may occur by a programmed process, apoptosis.
[22] In both prokaryotes and eukaryotes, DNA genomes are vulnerable to attack by reactive chemicals naturally produced in the intracellular environment and by agents from external sources.
An important internal source of DNA damage in both prokaryotes and eukaryotes is reactive oxygen species (ROS) formed as byproducts of normal aerobic metabolism.
[24] In the rat, which has a higher metabolic rate than humans, about 100,000 oxidative DNA damages occur per cell per day.