The mechanism of superoxide production by NADH:ubiquinone oxidoreductase (complex I) from bovine heart mitochondria

By L. Kussmaul, J. Hirst. Proceedings of the National Academy of Sciences of the United States of America, 2006

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View Paper: https://www.semanticscholar.org/paper/660d6a1b3d376dd546d69295f95aa17249caed44

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NAD(H) and NADP(H) Redox Couples and Cellular Energy Metabolism (2018, background): “ROS production by complex I requires a high NADH/ NAD ratio, whereas its dependence on proton motive force is controversial (1, 75, 105, 122, 132).”
Oxidative stress in the aging substantia nigra and the etiology of Parkinson's disease (2019, background): “Premature electron trans‐ fer from complexes I and III of the ETC to O2 occurs naturally in intact mammalian mitochondria (Drose & Brandt, 2008; Kussmaul & Hirst, 2006) and generates superoxide radicals (O2 −) as a physi‐ ological by‐product of energy production.”
Mitochondrial reactive oxygen species (ROS) and ROS-induced ROS release. (2014, background): “Some consider FMN (247, 256, 287, 345, 455), while others claim that iron-sulfur clusters N1a and N2 (142, 152, 186, 254), NAD radical (245), or ubisemiquinone (241) are responsible for O2 · generation in complex I.”
Mitochondrial Complex II Can Generate Reactive Oxygen Species at High Rates in Both the Forward and Reverse Reactions* (2012, background): “Of these, site IF in complex I and site IIIQo in complex III (9, 10, 12,13) have been investigated in greatest detail because of their ability to generate superoxide at high rates when they are fully or partially reduced.”
Mitochondrial proton and electron leaks (2010, background): “During forward electron fl ow with isolated mammalian complex I, redox titrations support the fully reduced fl avin of the FMN moiety as the source of O2 •− [32,33].”
ROS homeostasis and metabolism: a dangerous liason in cancer cells (2016, background): “The combined use of pro-oxidizing treatment and antioxidant inhibition is expected to cause severe oxidative stress and severe cytotoxicity Cell Death and Disease consequence of electron leakage during mitochondrial respiration using nicotinamide adenine dinucleotide (reduced form) (NADH) and FADH.1”