Complex I-mediated reactive oxygen species generation: modulation by cytochrome c and NAD(P)+ oxidation-reduction state.

By Yulia Kushnareva, A. Murphy, A. Andreyev. Biochemical Journal, 2002

675 citations recorded by the source corpus.

Subfields: Molecular Biology, Nutrition and Dietetics

View Paper: https://www.semanticscholar.org/paper/7c436485f42a026b6278846cb7d263fdc89c3134

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In Molecular Biology

1. M. Brand
2. M. Juhaszova
3. D. Zorov
4. Steven J. Sollott
5. M. Beal
6. S. Archer
7. Y. Bae
8. Hyunjin Oh

In Nutrition and Dietetics

1. M. Brand
2. J. Turrens

Citations in the corpus

• Mitochondria-Ros Crosstalk in the Control of Cell Death and Aging (2011, background): “It is a significant source of ROS [27] in particular O2−• [28] and H2O2 although whether or not Complex I is the major site of ROS production in intact mitochondria in vivo is a complicated issue.”
• The sites and topology of mitochondrial superoxide production (2010, background): “Rotenone (the complex I Q site inhibitor) markedly diminishes superoxide production (Gyulkhandanyan and Pennefather, 2004; Hansford et al., 1997; Kushnareva et al., 2002; Lambert and Brand, 2004b; Liu et al., 2002; Ohnishi et al., 2005; Votyakova and Reynolds, 2001), showing that large amounts of…”
• Molecular Mechanisms of Ischemia-Reperfusion Injury in Brain: Pivotal Role of the Mitochondrial Membrane Potential in Reactive Oxygen Species Generation (2012, background): “In complex I, two major sites of electron escape have been proposed, the flavoprotein component of electron entry into complex I [69] or the iron–sulfur cluster [70].”
• Mitochondrial reactive oxygen species (ROS) and ROS-induced ROS release. (2014, background): “(254) claimed that the ratio of NAD(P)H/ NAD(P) , rather than the level of NADH, determines reduction of ROS-producing sites in complex I.”
• Mechanism of Toxicity in Rotenone Models of Parkinson's Disease (2003, background): “There is a site of electron leak age in complex I upstream of the rotenone-binding site; partial inhibition of complex I, as produced by rotenone or as reported in PD, can enhance ROS production (Cassarino et al., 1997; Hensley et al., 1998; Barrientos and Moraes, 1999; Kushnareva et al., 2002).”
• Mitochondrial formation of reactive oxygen species (2003, background): “In Complex I, the primary source of O2 _• appears to be one of the iron–sulfur clusters (either N-1 a or N-2; Genova et al. 2001; Kushnareva et al. 2002).”
• Mitochondrial α-Ketoglutarate Dehydrogenase Complex Generates Reactive Oxygen Species (2004, background): “, 1997), has become available that is suitable for measurements with isolated mitochondria (Votyakova and Reynolds, 2001; Kushnareva et al., 2002).”
• A mitochondria-K+ channel axis is suppressed in cancer and its normalization promotes apoptosis and inhibits cancer growth. (2007, background): “…(Figures 2C and 2D), caused by DCA or molecular inhibition of PDK2 (Figure 7), increases the intramitochondrial production of the electron-donor NADH (Figure 3C), a substrate of the ETC complex I, leading to increased complex I-based ROS production (Figures 3B and 7B) (Kushnareva et al., 2002).”
• Regulation of reactive oxygen species generation in cell signaling (2011, methodology): “The superoxide at complex I is produced by two mechanisms: NADH-linked forward electron transport and succinate-linked reverse electron transport (Hansford et al., 1997; Kudin et al., 2004; Kushnareva et al., 2002; Kwong and Sohal, 1998; Lambert and Brand, 2004; Liu et al., 2002b; Votyakova and Reyn”
• Role of Oxidative Stress in Pathophysiology of Nonalcoholic Fatty Liver Disease (2018, background): “hydrogen peroxide (H2O2) than nondepleted mitochondria [33]; an impaired function of complex I-linked respiration, in a rodent model fed with choline-deficient diet, showed an abnormal ROS production [34].”