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A mitochondrion (pl. mitochondria) is an organelle found in the cells of most eukaryotes, such as animals, plants and fungi.Mitochondria have a double membrane structure and use aerobic respiration to generate adenosine triphosphate (ATP), which is used throughout the cell as a source of chemical energy. [2]
Mitochondrial DNA is a small portion of the DNA contained in a eukaryotic cell; most of the DNA is in the cell nucleus, and, in plants and algae, the DNA also is found in plastids, such as chloroplasts. [3] Human mitochondrial DNA was the first significant part of the human genome to be sequenced. [4]
Evidence suggests that mitochondria can also undergo fusion and exchange (in a form of crossover) genetic material among each other. Mitochondria sometimes form large matrices in which fusion, fission, and protein exchanges are constantly occurring. mtDNA shared among mitochondria (despite the fact that they can undergo fusion). [citation needed]
Mitochondrial disease is a group of disorders caused by mitochondrial dysfunction. Mitochondria are the organelles that generate energy for the cell and are found in every cell of the human body except red blood cells .
A new study explains how mitochondria act as “reservoirs” to store NAD for cells to use, which could help scientists come up with NAD-boosting therapies to combat aging and age-related diseases.
The glycerol-3-phosphate shuttle is a mechanism used in skeletal muscle and the brain [1] that regenerates NAD + from NADH, a by-product of glycolysis. NADH is a reducing equivalent that stores electrons generated in the cytoplasm during glycolysis. NADH must be transported into the mitochondria to enter the oxidative phosphorylation pathway.
Brain mitochondrial carrier protein 1 is a protein that in humans is encoded by the SLC25A14 gene. [ 5 ] [ 6 ] Mitochondrial uncoupling proteins (UCP) are members of the larger family of mitochondrial anion carrier proteins (MACP).
They impair the ability of mitochondria to make proteins, use oxygen, and produce energy. Researchers have not determined how changes in mitochondrial DNA lead to the specific signs and symptoms of MELAS. They continue to investigate the effects of mitochondrial gene mutations in different tissues, particularly in the brain. [9]