scholarly journals Reaction Rates and Mechanism of the Ascorbic Acid Oxidation by Molecular Oxygen Facilitated by Cu(II)-Containing Amyloid-β Complexes and Aggregates

2010 ◽  
Vol 114 (14) ◽  
pp. 4896-4903 ◽  
Author(s):  
Dianlu Jiang ◽  
Xiangjun Li ◽  
Lin Liu ◽  
Gargey B. Yagnik ◽  
Feimeng Zhou
Keyword(s):  
Ascorbic Acid ◽  
Molecular Oxygen ◽  
Amyloid Β ◽  
Reaction Rates ◽  
Acid Oxidation ◽  
Oxidation By Molecular Oxygen

Synthesis and evaluation of the influence of 5-sulfanyl-1,2,3-triazol-1-ylaminocarboxylic acid derivatives on kinetics of ascorbic acid oxidation

2016 ◽  
Vol 65 (1) ◽  
pp. 203-208 ◽  
Author(s):  
V. V. Emelianov ◽  
A. V. Musalnikova ◽  
E. A. Savateeva ◽  
Yu. S. Shakhmina ◽  
T. A. Kalinina ◽  
...  
Keyword(s):  
Ascorbic Acid ◽  
Acid Oxidation ◽  
Kinetics Of

II. Cytochrome P-450 enzymes and oxidative stress

2001 ◽  
Vol 281 (5) ◽  
pp. G1135-G1139 ◽  
Author(s):  
Graham Robertson ◽  
Isabelle Leclercq ◽  
Geoffrey C. Farrell
Keyword(s):  
Oxidative Stress ◽  
Fatty Acid ◽  
Molecular Oxygen ◽  
Hepatic Steatosis ◽  
Nonalcoholic Steatohepatitis ◽  
Acid Oxidation ◽  
Cellular Injury ◽  
Second Hit ◽  
Cytochrome P 450 ◽  
And Oxidative Stress

Oxidative stress is present in the liver of humans with steatosis and nonalcoholic steatohepatitis (NASH) and is a plausible mediator of cellular injury, inflammatory recruitment, and fibrogenesis. CYPs 2E1 and 4A are the microsomal oxidases involved with fatty acid oxidation. Both enzymes can reduce molecular oxygen to produce prooxidant species, which, if not countered efficiently by antioxidants, create oxidative stress. In this theme article, we present the evidence that, in the context of hepatic steatosis, CYPs 2E1 and 4A could generate the “second hit” of cellular injury, particularly when antioxidant reserves are depleted, and propose ways in which this could contribute to the pathogenesis of NASH.

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