The role of the hepatocellular redox state in the hepatic triglyceride accumulation following acute ethanol administration

1986 ◽  
Vol 35 (18) ◽  
pp. 3159-3164 ◽  
Author(s):  
Peter R. Ryle ◽  
Jagadish Chakraborty ◽  
Allan D. Thomson
Keyword(s):  
Redox State ◽  
Ethanol Administration ◽  
Hepatic Triglyceride ◽  
Triglyceride Accumulation ◽  
Acute Ethanol

scholarly journals The role of free serum tryptophan in the biphasic effect of acute ethanol administration on the concentrations of rat brain tryptophan, 5-hydroxytryptamine and 5-hydroxyindol-3-ylacetic acid

1976 ◽  
Vol 160 (2) ◽  
pp. 315-324 ◽  
Author(s):  
A A Badawy ◽  
M Evans
Keyword(s):  
Rat Brain ◽  
Tryptophan Metabolism ◽  
Ethanol Administration ◽  
Acute Administration ◽  
Free Tryptophan ◽  
Biphasic Effect ◽  
Acute Ethanol ◽  
Comparison Of The Results ◽  
Ylacetic Acid

1. Acute administration of ethanol exerts a biphasic effect on the concentrations of rat brain tryptophan, 5-hydroxytryptamine and 5-hydroxyindol-3-ylacetic acid. Both effects are associated with corresponding changes in the availability of circulating free tryptophan. 2. The initial increases in the above concentrations are prevented by ergotamine, are unaltered by allopurinol and are potentiated by theophylline, whereas the later decreases are prevented by both ergotamine and allopurinol. 3. It is suggested that the initial enhancement by ethanol of brain tryptophan metabolism is caused by catecholamine-mediated lipolysis followed by displacement of protein-bound serum tryptophan, whereas the activation of liver tryptophaan pyrrolase, which is produced by the same mechanism, leads to the later decreases in the brain concentrations of tryptophan and its metabolites. 4. The initial effects of ethanol can be reproduced by an equicaloric dose of sucrose, and a comparison of the two treatments alone could therefore be misleading. 5. The effects of ethanol on liver and brain tryptophan metabolism have also been examined in mice, and a comparison of the results with those previously reported suggests that the ethanol effects are strain-dependent.

Effects of Acute Ethanol Administration on Brain Oxidative Status: The Role of Acetaldehyde

2019 ◽  
Vol 43 (8) ◽  
pp. 1672-1681 ◽  
Author(s):  
Pablo Baliño ◽  
Ricard Romero-Cano ◽  
Juan Vicente Sánchez‐Andrés ◽  
Victoria Valls ◽  
Carlos González Aragón ◽  
...  
Keyword(s):  
Oxidative Status ◽  
Ethanol Administration ◽  
Acute Ethanol

Role of endotoxin in the hypermetabolic state after acute ethanol exposure

1998 ◽  
Vol 275 (6) ◽  
pp. G1252-G1258 ◽  
Author(s):  
Chantal A. Rivera ◽  
Blair U. Bradford ◽  
Vitor Seabra ◽  
Ronald G. Thurman
Keyword(s):  
Oxygen Uptake ◽  
Kupffer Cells ◽  
Ethanol Exposure ◽  
Ethanol Administration ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Hypermetabolic State ◽  
Acute Ethanol ◽  
Eicosanoid Release

This study investigated the role of endotoxin in the hypermetabolic state or swift increase in alcohol metabolism (SIAM) due to acute ethanol exposure. Female Sprague-Dawley rats (100–120 g) were given ethanol (5 g/kg) by gavage. Endotoxin measured in plasma from portal blood was not detectable in saline-treated controls; however, 90 min after ethanol, endotoxin was increased to 85 ± 14 pg/ml, and endotoxin clearance was diminished by ∼50%. Oxygen uptake in perfused livers was increased 48% by ethanol, and production of PGE2 by isolated Kupffer cells was increased similarly. These effects were blunted by elimination of gram-negative bacteria and endotoxin with antibiotics before ethanol administration. To reproduce ethanol-induced endotoxemia, endotoxin was infused via the mesenteric vein at a rate of 2 ng ⋅ kg−1 ⋅ h−1. Endotoxin mimicked the effect of ethanol on oxygen uptake. The specific Kupffer cell toxicant GdCl3completely prevented increases in oxygen uptake due to endotoxin. These findings demonstrate that endotoxin plays a pivotal role in SIAM, most likely by stimulating eicosanoid release from Kupffer cells.

Redox State in Atrial Fibrillation Pathogenesis and Relevant Therapeutic Approaches

2019 ◽  
Vol 26 (5) ◽  
pp. 765-779 ◽  
Author(s):  
Alexios S. Antonopoulos ◽  
Athina Goliopoulou ◽  
Evangelos Oikonomou ◽  
Sotiris Tsalamandris ◽  
Georgios-Angelos Papamikroulis ◽  
...  
Keyword(s):  
Atrial Fibrillation ◽  
Clinical Studies ◽  
Redox State ◽  
Redox Balance ◽  
Therapeutic Approaches ◽  
Critical Determinant ◽  
Electrophysiological Properties ◽  
Antioxidant Agents ◽  
Clinical Benefits

Background: Myocardial redox state is a critical determinant of atrial biology, regulating cardiomyocyte apoptosis, ion channel function, and cardiac hypertrophy/fibrosis and function. Nevertheless, it remains unclear whether the targeting of atrial redox state is a rational therapeutic strategy for atrial fibrillation prevention. Objective: To review the role of atrial redox state and anti-oxidant therapies in atrial fibrillation. Method: Published literature in Medline was searched for experimental and clinical evidence linking myocardial redox state with atrial fibrillation pathogenesis as well as studies looking into the role of redoxtargeting therapies in the prevention of atrial fibrillation. Results: Data from animal models have shown that altered myocardial nitroso-redox balance and NADPH oxidases activity are causally involved in the pathogenesis of atrial fibrillation. Similarly experimental animal data supports that increased reactive oxygen / nitrogen species formation in the atrial tissue is associated with altered electrophysiological properties of atrial myocytes and electrical remodeling, favoring atrial fibrillation development. In humans, randomized clinical studies using redox-related therapeutic approaches (e.g. statins or antioxidant agents) have not documented any benefits in the prevention of atrial fibrillation development (mainly post-operative atrial fibrillation risk). Conclusion: Despite strong experimental and translational data supporting the role of atrial redox state in atrial fibrillation pathogenesis, such mechanistic evidence has not been translated to clinical benefits in atrial fibrillation risk in randomized clinical studies using redox-related therapies.

scholarly journals Biogeochemical Controls on the Redox Evolution of Earth’s Oceans and Atmosphere

Elements ◽  
2020 ◽  
Vol 16 (3) ◽  
pp. 191-196 ◽  
Author(s):  
Christopher T. Reinhard ◽  
Noah J. Planavsky
Keyword(s):  
Redox State ◽  
Modeling Tools ◽  
Evolutionary Trajectory ◽  
Geochemical Tracers ◽  
Atmosphere System ◽  
Ocean Atmosphere ◽  
Dramatic Shift ◽  
Redox Evolution

The redox state of Earth’s atmosphere has undergone a dramatic shift over geologic time from reducing to strongly oxidizing, and this shift has been coupled with changes in ocean redox structure and the size and activity of Earth’s biosphere. Delineating this evolutionary trajectory remains a major problem in Earth system science. Significant insights have emerged through the application of redox-sensitive geochemical systems. Existing and emerging biogeochemical modeling tools are pushing the limits of the quantitative constraints on ocean–atmosphere redox that can be extracted from geochemical tracers. This work is honing our understanding of the central role of Earth’s biosphere in shaping the long-term redox evolution of the ocean–atmosphere system.

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