What are types of death? Will you give information about programmed death?
Submitted by on Wed, 01/07/2020 - 15:52
Dear Brother / Sister,
9.2.1-TYPES OF DEATH
In biology, cell death can basically be divided into two as programmed death (apoptosis and autophagy) and unprogrammed death (necrosis). However, in recent studies, it has been reported that there are other types of death that differ from apoptosis, autophagy and necrosis.1,2,3
9.2.2-Programmed Death (Apoptosis and Autophagy)
In programmed cell death (apoptosis), the cytoplasm condenses, the cell shrinks and contracts; its connection with neighboring cells breaks. Nuclear DNA breaks at nucleosomal regions. Cytochrome c is released from the mitochondrial membrane to the cytoplasm. The activity of proteolytic enzymes called caspases increases. The cell skeleton elements are broken down and rearranged on the cell surface. Ribosomes are in small groups and most of the endocytic vesicles are joined to the cell membrane. The mitochondrial task disappears in programmed cell death. Membrane vesicles are formed as a result of cell membrane changes. Inflammation does not occur since cytoplasmic vesicles (apoptotic bodies) containing nuclei and organelles are removed by phagocytic cells.4,5,6
The programmed death of the cell takes place in three stages:
1- Receiving the death signal (stimulation),
2- Caspase activation (Process)
3- Removal of the residues.
In programmed cell death,
a- First, death signal is received from inside or outside the cell.
b- Next, proteases (Caspases) are activated.
c- Activated caspases are assigned the task of destroying target proteins.
d- In the final stage of programmed death, apoptotic objects are formed and the resulting apoptotic objects are phagocytosed.
One type of death that is programmed but differs from apoptosis is autophagy. It is a physiologically programmed type of cell death that is responsible for the destruction of impaired organelles, damaged macromolecules and pathogens; it is independent of caspases and has no caspase activity. Autophagy is a miraculous incident that works as a quality control system in living beings.
Autophagy is a word that means “eating oneself”. It is the breakup of the structures inside itself to obtain energy when the cell is hungry.7,8
Autophagy is activated and the cell is killed when apoptosis is insufficient depending on the cell content. It is also known as a tumor suppressor mechanism.
Autophagic cell death protects homeostasis, especially by recycling intracellular molecules against hunger and all other stress factors. Thus, it is understood that autophagy has an important role in staying healthy and surviving.
If nutrients cannot be supplied to the cell, autophagy is activated, causing self-eating. Autophagy can also be triggered by cellular stress factors such as pathogen infection, toxin substances and hypoxia. Autophagy is actually a necessary mechanism to protect the cell in difficult conditions. However, if the pressure of the conditions causing stress increases, it consumes the cell and causes death. Disruption of autophagy mechanism causes cancer, early dementia, Alzheimer and various infections.
Autophagy is also an effective mechanism for the development of living beings (such as metamorphosis, wings in birds and palate formation in mammals).9 ATGs (Autophagy-related genes) are the genes assigned in autophagic cell death.10
It has been found that there are different types of cell deaths that are similar to apoptosis and autophagy (programmed cell death) in some aspects but different in terms of other aspects. For example, although the form of necroptosis is programmed death, it is similar to necrosis in some aspects.
1.Coşkun G. andÖzgür H., Arşiv 2011, 20, 145-158.
2.Tomatır A.G.T.,Klin J MedSci, 2003, 23, 499-508.
3.Yanıket al., Marmara Fen Bilimleri Dergisi, 2018, 1, 157-166.
4.Sharma et al., World Journal of Pharmaceutical Research, 2014, 3 (4), 1854-1872.
5.Öniz H., SSKTepecik Hast. Derg, 2004, 14 (1), 1-20.
6.Wyllie A.H.,Cancer MetastasRev., 1992, 11, 95-103.
7.Mizushima et al., Nature, 2008, 451, 1069-1075.
8.Karadağ A., Ankara Sağlık Hizmetleri Dergisi, 2016, 15 (2), 19-26.
9.Anding A. L. ve Baehrecke E.H.,Curr Top Dev Biol. 2015, 114, 67-91
10.Michaeliet al., Trends in Plant Science, 2016, 21 (2), 134-144.
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