Journal
EXPERIMENTAL GERONTOLOGY
Volume 45, Issue 7-8, Pages 466-472Publisher
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.exger.2010.01.003
Keywords
Reactive oxygen species; ROS; Electron transport; Semiquinone; Complex I; Complex III; Glycerol phosphate dehydrogenase; ETFQOR
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Funding
- NIA NIH HHS [P30 AG025708, R01 AG033542-01, P01 AG025901, P30 AG 025708, P01 AG 025901, R01 AG 033542, R01 AG033542, PL1 AG 032118, PL1 AG032118, P01 AG025901-03, P30 AG025708-05, PL1 AG032118-03] Funding Source: Medline
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Mitochondrial superoxide production is an important source of reactive oxygen species in cells, and may cause or contribute to ageing and the diseases of ageing. Seven major sites of superoxide production in mammalian mitochondria are known and widely accepted. In descending order of maximum capacity they are the ubiquinone-binding sites in complex I (site IQ) and complex III (site IIIQo), glycerol 3-phosphate dehydrogenase, the Flavin in complex I (site IF), the electron transferring flavoprotein:Q oxidoreductase (ETFQOR) of fatty acid beta-oxidation, and pyruvate and 2-oxoglutarate dehydrogenases. None of these sites is fully characterized and for some we only have sketchy information. The topology of the sites is important because it determines whether or not a site will produce superoxide in the mitochondrial matrix and be able to damage mitochondrial DNA. All sites produce superoxide in the matrix; site IIIQo and glycerol 3-phosphate dehydrogenase also produce superoxide to the intermembrane space. The relative contribution of each site to mitochondrial reactive oxygen species generation in the absence of electron transport inhibitors is unknown in isolated mitochondria, in cells or in vivo, and may vary considerably with species, tissue, substrate, energy demand and oxygen tension. (C) 2010 Elsevier Inc. All rights reserved.
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