An Introduction to Redox Balance and Lipid Oxidation

Author(s):  
Corinne Spickett ◽  
Maria Fedorova ◽  
Ralf Hoffmann ◽  
Henry Forman
2006 ◽  
Vol 20 (4) ◽  
Author(s):  
James Kenneth Friel ◽  
William Diehl‐Jones ◽  
Suh MiYoung ◽  
Vaibhav Shirwadkar

Diabetes ◽  
2019 ◽  
Vol 68 (Supplement 1) ◽  
pp. 165-LB
Author(s):  
ITZEL FLORES ◽  
CHRIS SHANNON ◽  
MARCEL FOURCAUDOT ◽  
TERRY BAKEWELL ◽  
LUKE NORTON

Diabetes ◽  
2020 ◽  
Vol 69 (Supplement 1) ◽  
pp. 1981-P
Author(s):  
AVIGDOR D. ARAD ◽  
FREDERICK J. DIMENNA ◽  
HANNAH D. KITTRELL ◽  
HARRY R. KISSILEFF ◽  
JEANINE ALBU

Diabetes ◽  
1987 ◽  
Vol 36 (11) ◽  
pp. 1341-1350 ◽  
Author(s):  
J. P. Felber ◽  
E. Ferrannini ◽  
A. Golay ◽  
H. U. Meyer ◽  
D. Theibaud ◽  
...  

Author(s):  
B.A. Katsnelson ◽  
M.P. Sutunkova ◽  
L.I. Privalova ◽  
S.N. Solovjeva ◽  
V.B. Gurvich ◽  
...  

The article presents in an experiment obtained principal results based on repeated low-level inhalation exposures of laboratory animals (white rats, outbred) to nickel oxide nanoparticles with a diameter of (23 ± 5) nm, 4 hours a day, 5 times a week for up to 10 months in a «nose only» installation. It was shown that non-specific body reactions to the action of NiO NPs include: diverse manifestations of systemic toxicity with a particularly pronounced influence on liver and kidney function, redox balance, damage to some areas of brain tissue, associated with proven movement of the nanoparticles themselves from the nasal mucosa along the olfactory tract; some cytological signs of probable development for allergic syndrome; paradoxically low severity of pulmonary pathology by pneumoconiotic type explained by a small chronic delay of nanoparticles in the lungs; the genotoxic effect of the organismal level, even at those low levels of chronic exposure, at which systemic toxicity is rather poorly. Along with that, NiO NPs also induce phase-stimulation of erythropoiesis, which is relatively specific for the toxic nickel effects.


2019 ◽  
Vol 26 (5) ◽  
pp. 765-779 ◽  
Author(s):  
Alexios S. Antonopoulos ◽  
Athina Goliopoulou ◽  
Evangelos Oikonomou ◽  
Sotiris Tsalamandris ◽  
Georgios-Angelos Papamikroulis ◽  
...  

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.


Author(s):  
EJ King ◽  
A Hugo ◽  
FH De Witt ◽  
HJ Van der Merwe ◽  
MD Fair

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