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Mitochondrial electron transport chain, ROS generation and . . . Under physiological conditions, 0 2-2% of the electrons in the ETC do not follow the normal transfer order but instead directly leak out of the ETC and interact with oxygen to produce superoxide or hydrogen peroxide (48,49)
Mitochondrial electron transport chain: Oxidative . . . The predominant route of ROS production by the ETC is the premature leak of electrons from complexes I, II, and III to mediate the one electron reduction of oxygen to superoxide (O 2 • −), which can then be dismutated to hydrogen peroxide (H 2 O 2) [6]
Electron Leak From the Mitochondrial Electron Transport Chain . . . In this study, we used complex‐specific electron leak suppressors to (1) identify which ETC complexes mediate DA O 2 sensing, and (2) determine whether changes in ROS, rather than metabolic inhibition, determine changes in DA tone
Mitochondrial electron transport chain, ROS generation and . . . The occurrence and development of a number of diseases are closely related to ROS overproduction Finally, proton leak and uncoupling proteins (UCPS) are discussed Proton leak consists of basal proton leak and induced proton leak Induced proton leak is precisely regulated and induced by UCPs
A Review on the Possible Leakage of Electrons through the . . . The finding of electron leakage during the electron transport within the mitochondrial membrane (in eukaryotes) or in the cell membrane of the prokaryotes is an important issue for the accumulation of the Reactive Oxygen Species (ROS) in the cytosol which in turn induce the probable aging of cells
Mitochondrial proton and electron leaks - PMC Mitochondrial proton and electron leak have a major impact on mitochondrial coupling efficiency and production of reactive oxygen species In the first part of this chapter, we address the molecular nature of the basal and inducible proton leak pathways, and their physiological importance
Frontiers | Mitochondrial Reactive Oxygen Species and Their . . . During the process of oxidative phosphorylation, electrons leak and interact with molecular oxygen to form superoxide (O − 2 2 - ) in complex I and complex III (which are the major ROS production site in the mitochondria) and complex II