Generation of reactive oxygen species by the mitochondrial electron transport chain

By Yuanbin Liu, G. Fiskum, D. Schubert. Journal of Neurochemistry, 2002

1,255 citations recorded by the source corpus.

Subfields: Molecular Biology, Physiology

View Paper: https://www.semanticscholar.org/paper/1b2fa107e688edab47037b8c4c3e52d4061607d1

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In Molecular Biology

1. M. Murphy
2. M. Beal
3. Y. Bae
4. S. Rhee
5. Hyunjin Oh
6. Young Do Yoo
7. P. Pinton
8. C. Giorgi

In Physiology

1. A. Hulbert
2. R. Pamplona
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Citations in the corpus

• The Impact of Oxidative Stress and Inflammation on RPE Degeneration in Non-neovascular AMD (2017, background): “Under physiological conditions during ATP synthesis, the ETC complexes generate ROS that leak out of the mitochondrial membrane (Chen et al., 2012; Liu et al., 2002; Murphy, 2009).”
• Regulation of reactive oxygen species generation in cell signaling (2011, background): “Moreover, the relationship between hydrogen peroxide (H2O2) and mammalian cell proliferation has been studied in different cell types (Caporossi et al., 2003; Chung et al., 2009; Liu et al., 2002a; Na et al., 2008; Sigaud et al., 2005; Stone and Collins, 2002; Stone and Yang, 2006).”
• Oxidative Stress, Prooxidants, and Antioxidants: The Interplay (2014, background): “Mitochondrion is the major cell organelle responsible for ROS production [50, 57].”
• How mitochondria produce reactive oxygen species (2008, background): “Under these conditions, the lowered (cid:2) p and the oxidized NADH pool prevent O 2 •− production by RET and greatly decrease O 2 •− production at the FMN of complex I, making H 2 O 2 efflux from mitochondria negligible compared with modes 1 or 2 (e.g. [4,78,89,119]).”
• Mitochondria-Ros Crosstalk in the Control of Cell Death and Aging (2011, background): “Because of this, succinate may promote ROS generation at Complex I level [6, 7].”
• Mitochondrial α-Ketoglutarate Dehydrogenase Complex Generates Reactive Oxygen Species (2004, background): “The finding that H2O2 production is frequently reported as being almost absent in the presence of succinate and rotenone (Barja, 1999; Liu et al., 2002) is intriguing because the intramitochondrial NADPH/NADP ratio under such conditions is high.”
• Calcium and apoptosis: ER-mitochondria Ca2+ transfer in the control of apoptosis (2008, background): “Protein kinases C can have a dual function in apoptosis, that is, the activation of specific PKC isoforms may protect or induce cell death, often in a cell-type-specific manner (Lavin et al., 1996; Liu et al., 2002; Griner and Kazanietz, 2007).”