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The Role of Mitochondria in Apoptosis

Ningthoujam Sandhyarani Sep 30, 2018
Mitochondria plays a major role in promoting apoptosis or programmed cell death, by releasing pro-apoptotic proteins in the cytoplasm. These proteins either activate caspases or inhibit other anti-apoptosis molecules, both of which lead to cell death.
Mitochondria (singular mitochondrion), the power house of the cell, are double membrane-bound cell organelles present in eukaryotes. Usually, they are either round or rod-shaped, with the size similar to bacteria. However, their shape and number may vary, depending on the type of the cell.
The major function of these organelles is to generate cellular energy in the form of adenosine triphosphate (ATP). Other than this, they are responsible for the signaling process, cell growth, differentiation, and cell death.
In the absence of mitochondria, a cell cannot regulate aerobic respiration, resulting in the death of the cell. Hence, it can be concluded that they are related to programmed cell death (PCD), called apoptosis, a factor responsible for the aging process.
Apoptosis, on the other hand, may occur due to injurious agents or inductions to undergo suicide. Whatever is the cause, an apoptotic cell shrinks and breaks into smaller bodies.

Mitochondria in Apoptosis

Apoptosis is a series of biochemical processes that involve mitochondria along with regulatory proteins and other signaling molecules. Mitochondria consist of molecules, which activate proteins in the cytoplasm, to undergo cellular programmed cell death.
These molecules are present in the intermembrane space of the organelles. In the cytoplasm, these molecules either block anti-apoptotic proteins or activate caspases (cysteine aspartate proteases). Both processes lead to cleavage of the nuclear DNA, thus resulting in cell death.
The process of apoptosis starts with oxidative stress and increased level of calcium ions in the cytoplasm. These cellular changes induce the opening of the mitochondrial permeability transition pore (PTP), which in turn, deactivates the organelle.
Following these signals, the organelles swell and release cytochrome c, through the pore. In these organelles, cytochrome c acts as a key protein for the electron transport in the respiratory processes.
As cytochrome c is transported in the cytoplasm, it initiates the mechanism of programmed cell death by activating caspases. The caspases are the proteins that cause cell death in the presence of cellular energy (ATP). In addition, there is another mitochondrial factor called AIF (apoptosis inducing factor), a molecule, which is released in the cytoplasm.
According to studies, it is found that AIF mediated apoptosis is independent of the caspases regulation. The programmed cell death resulted from AIF, plays an important role in the development of an organism. The release of molecules by mitochondria is controlled by Bcl-2, like proteins and ion channels.
Overall, the role of mitochondria in programmed cell death, includes a change in cellular oxidation-reduction, loss of membrane potential (permeability), alteration in electron transport, release of AIF and cytochrome c (that acts as caspase activator).
Apoptosis is not harmful to the organism, rather it serves the main purpose of disposing cellular debris. Research studies revealed that in an adult human body, about 50-70 billion cells die daily due to this phenomenon.
However, a disorder in programmed cell death, either insufficient or excess, may lead to the development of certain diseases. For example, a low rate results in unmanageable cell proliferation, leading to cancer, whereas a high rate causes hypotrophy.