Mitochondria Research Paper

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Mitochondria are sub-cellular organelles which are found suspended in the cytoplasm of majority of eukaryotic cells. One of their functions is to produce energy in a form (ATP) that is useful for all cells to maintain the intra and extra cellular functioning. Mitochondrion has a matrix that is surrounded by two membranes called the inner membrane and the outer membrane. These two membranes are separated by an inter membrane space. The outer membrane has proteins embedded in them (most of which are porins- proteins that allow free transfer of molecules such as nutrients, ions, proteins etc.). While the outer membrane is smooth, the inner membrane is highly convoluted into structures called cristae to increase the surface area of the membrane. [1]
Cytochrome c is an important protein belonging to the cytochrome family. It is found within the mitochondria matrix. It helps in the process of electron transport chain (ETC). [2]
Mitochondria synthesises its own protein which are released in response to various apoptotic stimuli. These proteins promote apoptosis by activating caspases and nucleases or by neutralizing cytosolic inhibitors of this process.[3]
Viruses have been long considered to be a living organism. They have their own DNA which makes it a debatable issue of whether or not to categorize them as living. They require energy to replicate/ survive within a host cell and so they take control of various organelles including mitochondria. [1]
In the case of a fatal disease like cancer, the treatment causes chemotherapy induced peripheral neuropathy (CIPN). Oxidative stress mediated nerve damage also the mitochondrial dysfunctions are pivotal pathogenic mechanisms contributing to CIPN. [3]
Cell Apoptosis:
Apoptosis is programmed ...

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...tible to oxidative stress due to the high concentration of phospholipids, mitochondria rich axoplasm and weak cellular antioxidant protection in them.
The physical damage to neural cells ultimately lead to oxidative stress and so mitochondrial dysfunction. Oxidative damage to peripheral neurons can cause damage to myelin sheath, mitochondrial proteins and other antioxidant enzymes.
It’s proposed by many experiments that mitochondrial dysfunction contributes to neuropathic symptoms which are produced by various chemotherapeutic agents. It is suggested that neural apoptosis maybe through the intrinsic pathway or extrinsic.
The accumulation of dysfunctional mitochondria because of inefficient removal of damaged mitochondria (mitophagy) causes an increase in free radical leakiness and the cycle of oxidative damage to the bio molecules and thus helping in apoptosis. [3]

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