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Overview of mitochondrial Reactive Oxygen Species (ROS) Production

ROS production by mitochondria can lead to oxidative damage to mitochondrial proteins, membranes and DNA, impairing the ability of mitochondria to synthesize ATP and to carry out their wide range of metabolic functions, including the tricarboxylic acid cycle, fatty acid oxidation, the urea cycle, amino acid metabolism, haem synthesis and FeS centre assembly that are central to the normal operation of most cells.

Mitochondrial oxidative damage can also increase the tendency of mitochondria to release intermembrane space proteins such as cytochrome c (cyt c) to the cytosol by mitochondrial outer membrane permeabilization (MOMP) and thereby activate the cell's apoptotic machinery.

In addition, mitochondrial ROS production leads to induction of the mitochondrial permeability transition pore (PTP), which renders the inner membrane permeable to small molecules in situations such as ischaemia/reperfusion injury.

Consequently, it is unsurprising that mitochondrial oxidative damage contributes to a wide range of pathologies. In addition, mitochondrial ROS may act as a modulatable redox signal, reversibly affecting the activity of a range of functions in the mitochondria, cytosol and nucleus.

Reference

Michael P Murphy How mitochondria produce reactive oxygen species. Biochem. J.: 2009, 417(1);1-13 PubMed 19061483


Copyright

© 2009 The Author(s) The author(s) has paid for this article to be freely available under the terms of the Creative Commons Attribution Non-Commercial Licence (http://creativecommons.org/licenses/by-nc/2.5/) which permits unrestricted non-commercial use, distribution and reproduction in any medium, provided the original work is properly cited.

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current07:57, 20 March 2009Thumbnail for version as of 07:57, 20 March 2009453 × 477 (124 KB)S8600021 (talk | contribs)Figure 1 Overview of mitochondrial ROS production ROS production by mitochondria can lead to oxidative damage to mitochondrial proteins, membranes and DNA, impairing the ability of mitochondria to synthesize ATP and to carry out their wide range of metab
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