scholarly journals Inactivation of the Na+ -translocating NADH:ubiquinone oxidoreductase from Vibrio alginolyticus by reactive oxygen species

2002 ◽  
Vol 269 (4) ◽  
pp. 1287-1292 ◽  
Author(s):  
Julia Steuber ◽  
Michèle Rufibach ◽  
Günter Fritz ◽  
Frank Neese ◽  
Peter Dimroth
Keyword(s):  
Reactive Oxygen Species ◽  
Reactive Oxygen ◽  
Vibrio Alginolyticus ◽  
Nadh:Ubiquinone Oxidoreductase ◽  
Oxygen Species

scholarly journals Production of Reactive Oxygen Species by Complex I (NADH:Ubiquinone Oxidoreductase) from Escherichia coli and Comparison to the Enzyme from Mitochondria†

Biochemistry ◽  
2008 ◽  
Vol 47 (12) ◽  
pp. 3964-3971 ◽  
Author(s):  
Daria Esterházy ◽  
Martin S. King ◽  
Gregory Yakovlev ◽  
Judy Hirst
Keyword(s):  
Escherichia Coli ◽  
Reactive Oxygen Species ◽  
Complex I ◽  
Reactive Oxygen ◽  
Nadh:Ubiquinone Oxidoreductase ◽  
Oxygen Species

scholarly journals Reduction of Hydrophilic Ubiquinones by the Flavin in Mitochondrial NADH:Ubiquinone Oxidoreductase (Complex I) and Production of Reactive Oxygen Species†

Biochemistry ◽  
2009 ◽  
Vol 48 (9) ◽  
pp. 2053-2062 ◽  
Author(s):  
Martin S. King ◽  
Mark S. Sharpley ◽  
Judy Hirst
Keyword(s):  
Reactive Oxygen Species ◽  
Complex I ◽  
Reactive Oxygen ◽  
Nadh:Ubiquinone Oxidoreductase ◽  
Oxygen Species

Resonance Raman Spectral Properties of FMN of Bovine Heart NADH:ubiquinone Oxidoreductase Suggesting a Mechanism for the Prevention of Spontaneous Production of Reactive Oxygen Species

Biochemistry ◽  
2012 ◽  
Vol 52 (1) ◽  
pp. 98-104 ◽  
Author(s):  
Masahide Hikita ◽  
Kyoko Shinzawa-Itoh ◽  
Masakazu Moriyama ◽  
Takashi Ogura ◽  
Kiyohito Kihira ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Spectral Properties ◽  
Resonance Raman ◽  
Reactive Oxygen ◽  
Nadh:Ubiquinone Oxidoreductase ◽  
Oxygen Species ◽  
Bovine Heart ◽  
Spontaneous Production ◽  
Raman Spectral

The production of reactive oxygen species by complex I

2008 ◽  
Vol 36 (5) ◽  
pp. 976-980 ◽  
Author(s):  
Judy Hirst ◽  
Martin S. King ◽  
Kenneth R. Pryde
Keyword(s):  
Reactive Oxygen Species ◽  
Complex I ◽  
Neuromuscular Diseases ◽  
Reactive Oxygen ◽  
Flavin Mononucleotide ◽  
Nadh:Ubiquinone Oxidoreductase ◽  
Oxygen Species ◽  
Quinone Binding ◽  
O2 Reduction ◽  
Reverse Electron Transport

ROS (reactive oxygen species) are considered to be a major cause of cellular oxidative stress, linked to neuromuscular diseases and aging. Complex I (NADH:ubiquinone oxidoreductase) is one of the main contributors to superoxide production by mitochondria, and knowledge of its mechanism of O2 reduction is required for the formulation of causative connections between complex I defects and pathological effects. There is evidence for two distinct (but not mutually exclusive) sites of O2 reduction by complex I. Studies of the isolated enzyme largely support the participation of the reduced flavin mononucleotide in the active site for NADH oxidation, and this mechanism is supported in mitochondria by correlations between the NAD(P)+ potential and O2 reduction. In addition, studies of intact mitochondria or submitochondrial particles have suggested a mechanism involving the quinone-binding site, supported by observations during reverse electron transport and the use of ‘Q-site’ inhibitors. Here, we discuss extant data and models for O2 reduction by complex I. We compare results from the isolated enzyme with results from intact mitochondria, aiming to identify similarities and differences between them and progress towards combining them to form a single, unified picture.

Mitochondria as a source of reactive oxygen species

2009 ◽  
pp. c3 ◽  
Author(s):  
Helena M. Cochemé ◽  
Michael P. Murphy
Keyword(s):  
Reactive Oxygen Species ◽  
Reactive Oxygen ◽  
Oxygen Species

Clinical aspects of reactive oxygen and nitrogen species

2004 ◽  
Vol 71 ◽  
pp. 121-133 ◽  
Author(s):  
Ascan Warnholtz ◽  
Maria Wendt ◽  
Michael August ◽  
Thomas Münzel
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Risk Factor ◽  
Endothelial Dysfunction ◽  
Vascular Tissue ◽  
Rapid Development ◽  
Reactive Oxygen ◽  
Clinical Aspects ◽  
No Production ◽  
Oxygen Species

Endothelial dysfunction in the setting of cardiovascular risk factors, such as hypercholesterolaemia, hypertension, diabetes mellitus and chronic smoking, as well as in the setting of heart failure, has been shown to be at least partly dependent on the production of reactive oxygen species in endothelial and/or smooth muscle cells and the adventitia, and the subsequent decrease in vascular bioavailability of NO. Superoxide-producing enzymes involved in increased oxidative stress within vascular tissue include NAD(P)H-oxidase, xanthine oxidase and endothelial nitric oxide synthase in an uncoupled state. Recent studies indicate that endothelial dysfunction of peripheral and coronary resistance and conductance vessels represents a strong and independent risk factor for future cardiovascular events. Ways to reduce endothelial dysfunction include risk-factor modification and treatment with substances that have been shown to reduce oxidative stress and, simultaneously, to stimulate endothelial NO production, such as inhibitors of angiotensin-converting enzyme or the statins. In contrast, in conditions where increased production of reactive oxygen species, such as superoxide, in vascular tissue is established, treatment with NO, e.g. via administration of nitroglycerin, results in a rapid development of endothelial dysfunction, which may worsen the prognosis in patients with established coronary artery disease.

Fas ligand expression in rat kupffer cells in response to lipopolysaccharide is mediated by reactive oxygen species

2001 ◽  
Vol 120 (5) ◽  
pp. A361-A361
Author(s):  
K UCHIKURA ◽  
T WADA ◽  
Z SUN ◽  
S HOSHINO ◽  
G BULKLEY ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Kupffer Cells ◽  
Fas Ligand ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Ligand Expression
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