Abstract
Reactive oxygen species (ROS) are highly reactive reduced oxygen molecules that result from aerobic metabolism. The common forms are the superoxide anion (O2∙−) and hydrogen peroxide (H2O2) and their derived forms, hydroxyl radical (HO∙) and hydroperoxyl radical (HOO∙). Their production sites in mitochondria are reviewed. Even though being highly toxic products, ROS seem important in transducing information from dysfunctional mitochondria. Evidences of signal transduction mediated by ROS in mitochondrial deficiency contexts are then presented in different organisms such as yeast, mammals or photosynthetic organisms.
Highlights
Evidences of signal transduction mediated by reactive oxygen species (ROS) in mitochondrial deficiency contexts are presented in different organisms such as yeast, mammals or photosynthetic organisms
NADH and succinate produced by the Krebs cycle are oxidised by complex I (NADH:ubiquinone oxidoreductase) and complex II respectively and the electrons are transferred to the ubiquinone pool, leading to the reduction of ubiquinone to ubiquinol inside the mitochondrial membrane
Electrons are transferred by complex III from ubiquinol to cytochrome c, a soluble electron carrier located in the intermembrane space, and from cytochrome c to molecular oxygen (O2) via complex IV
Summary
Reactive oxygen species (ROS) are highly reactive reduced oxygen molecules that result from aerobic metabolism. The common forms are the superoxide anion (O2−) and hydrogen peroxide (H2O2) and their derived forms, hydroxyl radical (HO) and hydroperoxyl radical (HOO). Their production sites in mitochondria are reviewed. Even though being highly toxic products, ROS seem important in transducing information from dysfunctional mitochondria. Evidences of signal transduction mediated by ROS in mitochondrial deficiency contexts are presented in different organisms such as yeast, mammals or photosynthetic organisms
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