Abstract: Oxidative Stress, Disease and Cancer, pp. 1-60 (2006) No AccessYin and Yang of Mitochondrial ROSAnatoly Starkov and Kendall B. WallaceAnatoly StarkovNeurology and Neuroscience, Weill Medical College, Cornell University, A501, 445 E 69th Street, New York, NY 10021, USA and Kendall B. WallaceDepartment of Biochemistry and Molecular Biology, University of Minnesota School of Medicine, 1035 University Drive, Duluth, MN 55812, USAhttps://doi.org/10.1142/9781860948046_0001Cited by:1 PreviousNext AboutSectionsPDF/EPUB ToolsAdd to favoritesDownload CitationsTrack CitationsRecommend to Library ShareShare onFacebookTwitterLinked InRedditEmail Abstract: The following sections are included: Introduction Multiplicity of ROS-Producing Sources in Mitochondria ROS Production at Complex I of Mitochondrial Respiratory Chain Q-Cycle and the Mechanism of ROS Production at Complex III The Q-cycle model of the coenzyme Q oxidation The site and source of electrons for the superoxide formation The unexplained features of the superoxide production mechanism at the Complex III The mechanism of superoxide production at Complex III Mitochondrial ROS Detoxifying Systems Membrane lipid peroxide removal systems Phospholipids hydroperoxide glutathione peroxidase Superoxide Removal Systems MnSOD Cytochrome c Hydrogen Peroxide Removal Systems Catalase Glutathione Glutathione-S-transferase Glutathione reductase A quintessence of the GSH-dependent mitochondrial ROS-defense network Hypothetical antioxidant function of NAD(P)H Glutathione peroxidase Peroxiredoxins and other oxins Mitochondrial ROS Production in Pathologies Types of mechanisms enhancing mitochondrial ROS production Complex I as a site of enhanced ROS production Complex III as a site of enhanced ROS production ATPase mutation may enhance ROS production Ischemia reperfusion enhances mitochondrial ROS production Mitochondrial Ca2+ accumulation per se unlikely enhances ROS production Ca2+-induced mitochondrial permeability transition may be responsible for an increase in ROS production Postscriptum References FiguresReferencesRelatedDetailsCited By 1Zinc oxide nanoparticles induced gene mutation at the HGPRT locus and cell cycle arrest associated with apoptosis in V‐79 cellsAbhishek Kumar Jain, Divya Singh, Kavita Dubey, Renuka Maurya and Alok Kumar Pandey7 January 2019 | Journal of Applied Toxicology, Vol. 39, No. 5 Oxidative Stress, Disease and CancerMetrics History PDF download
Publication Year: 2006
Publication Date: 2006-04-01
Language: en
Type: book-chapter
Indexed In: ['crossref']
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Cited By Count: 5
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