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Mitochondrial Management of Reactive Oxygen Species

Journal

ANTIOXIDANTS
Volume 10, Issue 11, Pages -

Publisher

MDPI
DOI: 10.3390/antiox10111824

Keywords

oxygen consumption; OxPhos; ROS generation; ROS removal; enzymatic antioxidants; low-molecular-weight antioxidants

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Mitochondria in aerobic eukaryotic cells not only produce energy but also harmful substances such as ROS, and possess an efficient antioxidant system to detoxify these substances. As ROS production increases, mitochondria are damaged and release more harmful substances, but their antioxidant system can detoxify exogenous ROS at the expense of reducing the equivalents generated in mitochondria.
Mitochondria in aerobic eukaryotic cells are both the site of energy production and the formation of harmful species, such as radicals and other reactive oxygen species, known as ROS. They contain an efficient antioxidant system, including low-molecular-mass molecules and enzymes that specialize in removing various types of ROS or repairing the oxidative damage of biological molecules. Under normal conditions, ROS production is low, and mitochondria, which are their primary target, are slightly damaged in a similar way to other cellular compartments, since the ROS released by the mitochondria into the cytosol are negligible. As the mitochondrial generation of ROS increases, they can deactivate components of the respiratory chain and enzymes of the Krebs cycle, and mitochondria release a high amount of ROS that damage cellular structures. More recently, the feature of the mitochondrial antioxidant system, which does not specifically deal with intramitochondrial ROS, was discovered. Indeed, the mitochondrial antioxidant system detoxifies exogenous ROS species at the expense of reducing the equivalents generated in mitochondria. Thus, mitochondria are also a sink of ROS. These observations highlight the importance of the mitochondrial antioxidant system, which should be considered in our understanding of ROS-regulated processes. These processes include cell signaling and the progression of metabolic and neurodegenerative disease.

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