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Damaged mitochondria cause a depletion in ATP and a release of cytochrome c, which leads to activation of caspases and onset of apoptosis. Mitochondrial damage is not caused solely by oxidative stress or disease processes; normal mitochondria will eventually accumulate oxidative damage hallmarks overtime, which can be deleterious to ...
Mitophagy is the selective degradation of mitochondria by autophagy. It often occurs to defective mitochondria following damage or stress. Mitophagy promotes the turnover of mitochondria and prevents the accumulation of dysfunctional mitochondria which can lead to cellular degeneration.
Cell damage (also known as cell injury) is a variety of changes of stress that a cell suffers due to external as well as internal environmental changes. Amongst other causes, this can be due to physical, chemical, infectious, biological, nutritional or immunological factors. Cell damage can be reversible or irreversible.
However, if this molecule can activate or restore parkin function, it could help remove damaged mitochondria even in later stages, potentially slowing disease progression and improving cell health.
Mitochondria are dynamic organelles with the ability to fuse and divide , forming constantly changing tubular networks in most eukaryotic cells. These mitochondrial dynamics, first observed over a hundred years ago [ 1 ] are important for the health of the cell, and defects in dynamics lead to genetic disorders .
The term "Reverse electron transfer" is used in regard to the reversibility of the reaction performed by complex I of the mitochondrial or bacterial respiratory chain. Complex I is responsible for the oxidation of NADH generated in catabolism when in the forward reaction electrons from the nucleotide (NADH) are transferred to membrane ...
Mitochondrial toxicity is a condition in which the mitochondria of a body's cells become damaged or decline significantly in number; it occurs as a side effect of certain antiretroviral drugs used to treat human immunodeficiency virus, or HIV. [1]
He found ROS as the main cause of damage to macromolecules, known as "ageing". He later modified his theory because he found that mitochondria were producing and being damaged by ROS, leading him to the conclusion that mitochondria determine ageing. In 1972, he published his theory in the Journal of the American Geriatrics Society. [20]