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・ Mitochondrial fusion
・ Mitochondrial intermediate peptidase
・ Mitochondrial intermembrane space
・ Mitochondrial matrix
・ Mitochondrial membrane transport protein
・ Mitochondrial myopathy
・ Mitochondrial neurogastrointestinal encephalopathy syndrome
・ Mitochondrial optic neuropathies
・ Mitochondrial permeability transition pore
・ Mitochondrial processing peptidase
・ Mitochondrial protein-transporting ATPase
・ Mitochondrial pyruvate carrier 2
・ Mitochondrial ribosomal death-associated protein 3
・ Mitochondrial ribosomal protein L41
・ Mitochondrial ribosomal protein L42
Mitochondrial ROS
・ Mitochondrial shuttle
・ Mitochondrial toxicity
・ Mitochondrial translational release factor 1
・ Mitochondrial trifunctional protein
・ Mitochondrial trifunctional protein deficiency
・ Mitochondrial tRNA pseudouridine27/28 synthase
・ Mitochondrion
・ Mitochondrion (band)
・ Mitocu Dragomirnei
・ Mitocu River
・ Mitoferrin-1
・ Mitogaku
・ Mitogen
・ Mitogen-activated protein kinase


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Mitochondrial ROS : ウィキペディア英語版
Mitochondrial ROS

Mitochondrial ROS (mtROS or mROS) are reactive oxygen species (ROS) that are produced by mitochondria. Generation of mitochondrial ROS mainly takes place at the electron transport chain located on the inner mitochondrial membrane during the process of oxidative phosphorylation (OXPHOS). Leakage of electrons at complex I and complex III from electron transport chains leads to partial reduction of oxygen to form superoxide. Subsequently, superoxide is quickly dismutated to hydrogen peroxide by two dismutases including superoxide dismutase 2 (SOD2) in mitochondrial matrix and superoxide dismutase 1 (SOD1) in mitochondrial intermembrane space. Collectively, both superoxide and hydrogen peroxide generated in this process are considered as mitochondrial ROS.
Once thought as merely the by-products of cellular metabolism, mitochondrial ROS are increasingly viewed as important signaling molecules. At low levels, mitochondrial ROS are considered to be important for metabolic adaptation as seen in hypoxia. Moderate levels of mitochondrial ROS, stimulated by danger signals such as Toll-like receptor 4 ligand bacterial endotoxin lipopolysaccharide (LPS), are involved in regulating inflammatory response. Finally, high levels of mitochondrial ROS activate apoptosis/autophagy pathways capable of inducing cell death.
== References ==



抄文引用元・出典: フリー百科事典『 ウィキペディア(Wikipedia)
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