Identification of cell death

This description is more functional and applies to both in vitro and in vivo, so cell death subroutines are now described by a series of precise, measurable, biochemical features.

Necrosis is an unprogrammed death of cells, which involves early plasma membrane changes leading to loss of calcium and sodium imbalance.

There are also mitochondrial changes which include calcium overload and activation of phospholipases leading to membrane diffusion signals, a stage of irreversible damage.

The secondary stage involves swelling of the lysosome, dilation of the endoplasmic reticulum, a leakage of enzymes and proteins and a loss of compartmentalization.

Apoptosis, or programmed cell death, is generally characterized by distinct morphological characteristics and energy-dependent biochemical mechanisms.

[2] This method was observed by Attalah and Johnson who used electronic particle analyses to determine cell viability.

When the cell died the nucleus went through destruction stages, one of them pyknosis, which lead to the release of a basic histone group and this happened when the irreversible condensation of chromatins occurred.

The phagocytosis process took place in secondary lysosomes and the autophagy and heterophagy controlled the dead cell by acid hydrolysis activity.

The result of this experiment is the red color which is caused by azo-dye technique done above and this is an indicator that cell autolysis occurred.

Incorporate tritiated thymidine gives silver grains in the photographic emulsion which happened in the cell nuclei.

This was concluded after some attempts from the scientists like Kerr (1972) who proposed the general concept of apoptosis in vertebrates, While Scheweichel and Merker (1973) described induced and physiological cell death in prenatal mouse tissues.

Many authors show that there may be a premonitory increase in protein synthesis as a primer for programmed cell death.