scholarly journals The role of aldehyde oxidase in ethanol-induced hepatic lipid peroxidation in the rat

1990 ◽  
Vol 268 (3) ◽  
pp. 579-583 ◽  
Author(s):  
S Shaw ◽  
E Jayatilleke
Keyword(s):  
Lipid Peroxidation ◽  
Free Radicals ◽  
Liver Injury ◽  
Xanthine Oxidase ◽  
Aldehyde Oxidase ◽  
Ethanol Metabolism ◽  
Dependent Manner ◽  
Hepatic Lipid ◽  
Hepatic Lipid Peroxidation

Hepatic lipid peroxidation has been implicated in the pathogenesis of alcohol-induced liver injury, but the mechanism(s) by which ethanol metabolism or resultant free radicals initiate lipid peroxidation is not fully defined. The role of the molybdenum-containing enzymes aldehyde oxidase and xanthine oxidase in the generation of such free radicals was investigated by measuring alkane production (lipoperoxidation products) in isolated rat hepatocytes during ethanol metabolism. Inhibition of aldehyde oxidase and xanthine oxidase (by feeding tungstate at 100 mg/day per kg) decreased alkane production (80-95%), whereas allopurinol (20 mg/kg by mouth), a marked inhibitor of xanthine oxidase, inhibited alkane production by only 35-50%. Addition of acetaldehyde (0-100 microM) (in the presence of 50 microM-4-methylpyrazole) increased alkane production in a dose-dependent manner (Km of aldehyde oxidase for acetaldehyde 1 mM); menadione, an inhibitor of aldehyde oxidase, virtually inhibited alkane production. Desferrioxamine (5-10 microM) completely abolished alkane production induced by both ethanol and acetaldehyde, indicating the importance of catalytic iron. Thus free radicals generated during the metabolism of acetaldehyde by aldehyde oxidase may be a fundamental mechanism in the initiation of alcohol-induced liver injury.

Hepatic lipid peroxidation in hereditary hemochromatosis and alcoholic liver injury

1999 ◽  
Vol 133 (5) ◽  
pp. 451-460 ◽  
Author(s):  
Onni Niemelä ◽  
Seppo Parkkila ◽  
Robert S. Britton ◽  
Elizabeth Brunt ◽  
Christine Janney ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Liver Injury ◽  
Hereditary Hemochromatosis ◽  
Alcoholic Liver Injury ◽  
Hepatic Lipid ◽  
Hepatic Lipid Peroxidation

Role of Free Radicals and Lipid Peroxidation in Gastric Mucosal Injury Induced by Ischemia-Reperfusion in Rats

1989 ◽  
Vol 24 (sup162) ◽  
pp. 55-58 ◽  
Author(s):  
S. Ueda ◽  
T. Yoshikawa ◽  
S. Takahashi ◽  
H. Ichikawa ◽  
M. Yasuda ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Free Radicals ◽  
Ischemia Reperfusion ◽  
Mucosal Injury ◽  
Gastric Mucosal Injury

Free radicals in hypoxic rat diaphragm contractility: no role for xanthine oxidase

2001 ◽  
Vol 281 (6) ◽  
pp. L1402-L1412 ◽  
Author(s):  
Leo M. A. Heunks ◽  
Herwin A. Machiels ◽  
Ronney de Abreu ◽  
Xiao Ping Zhu ◽  
Henricus F. M. van der Heijden ◽  
...  
Keyword(s):  
Free Radicals ◽  
Xanthine Oxidase ◽  
Power Output ◽  
Harmful Effect ◽  
Force Generation ◽  
Muscle Performance ◽  
Rat Diaphragm ◽  
Shortening Velocity ◽  
Contraction Pattern

Recent evidence indicates that hypoxia enhances the generation of oxidants. Little is known about the role of free radicals in contractility of the rat diaphragm during hypoxia. We hypothesized that antioxidants improve contractility of the hypoxic rat diaphragm and that xanthine oxidase (XO) is an important source of free radicals in the hypoxic diaphragm. The effects of N-acetylcysteine (NAC; 18 mM), Tiron (10 mM), and the XO inhibitor allopurinol (250 μM) were studied on isometric and isotonic force generation during hypoxia (Po 2 ∼7 kPa). NAC and Tiron decreased maximal force generation, slowed the shortening velocity, and decreased the power output. Fatigue rate was decreased in the presence of either NAC or Tiron. Allopurinol did not alter the contractility or fatigability of the diaphragm. During hyperoxia (Po 2 ∼85 kPa), neither NAC nor allopurinol affected the contractility or fatigability of the diaphragm. Thus free radicals play a significant role in diaphragm contractility during hypoxia. Whether antioxidants exert a beneficial or harmful effect on muscle performance depends on the contraction pattern of the muscle. Free radicals generated by XO do not play a role in diaphragm contractility during either hypoxia or hyperoxia.

scholarly journals Bariatric Surgery-Induced Weight Loss Reduces Hepatic Lipid Peroxidation Levels and Affects Hepatic Cytochrome P-450 Protein Content

2010 ◽  
Vol 251 (6) ◽  
pp. 1041-1048 ◽  
Author(s):  
Lauren N. Bell ◽  
Constance J. Temm ◽  
Rashmil Saxena ◽  
Raj Vuppalanchi ◽  
Philip Schauer ◽  
...  
Keyword(s):  
Bariatric Surgery ◽  
Lipid Peroxidation ◽  
Weight Loss ◽  
Protein Content ◽  
Hepatic Lipid ◽  
Hepatic Lipid Peroxidation ◽  
Cytochrome P 450 ◽  
Hepatic Cytochrome

scholarly journals 4-HNE Immunohistochemistry and Image Analysis for Detection of Lipid Peroxidation in Human Liver Samples Using Vitamin E Treatment in NAFLD as a Proof of Concept

2020 ◽  
Vol 68 (9) ◽  
pp. 635-643 ◽  
Author(s):  
Maren C. Podszun ◽  
Joon-Yong Chung ◽  
Kris Ylaya ◽  
David E. Kleiner ◽  
Stephen M. Hewitt ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Image Analysis ◽  
Vitamin E ◽  
Dynamic Range ◽  
Clinical Diagnostics ◽  
Automated Image Analysis ◽  
Antioxidant Vitamin ◽  
Alcoholic Fatty Liver ◽  
Hepatic Lipid ◽  
Hepatic Lipid Peroxidation

Lipid peroxidation is a common feature of liver diseases, especially non-alcoholic fatty liver disease (NAFLD). There are limited validated tools to study intra-hepatic lipid peroxidation, especially for small specimen. We developed a semi-quantitative, fully automated immunohistochemistry assay for the detection of 4-hydroxynoneal (4-HNE) protein adducts, a marker of lipid peroxidation, for adaptation to clinical diagnostics and research. We used Hep G2 cells treated with 4-HNE to validate specificity, sensitivity, and dynamic range of the antibody. Staining and semi-quantitative automated readout were confirmed in human needle-biopsy liver samples from subjects with NAFLD and normal liver histology. The ability to detect changes in lipid peroxidation was tested in paired liver biopsies from NAFLD subjects, obtained before and after 4 weeks of treatment with the antioxidant vitamin E (ClinicalTrials.gov NCT01792115, n=21). The cellular calibrator was linear and NAFLD patients had significantly higher levels of 4-HNE adducts compared to controls ( p=0.02). Vitamin E treatment significantly decreased 4-HNE ( p=0.0002). Our findings demonstrate that 4-HNE quantification by immunohistochemistry and automated image analysis is feasible and able to detect changes in hepatic lipid peroxidation in clinical trials. This method can be applied to archival and fresh samples and should be considered for use in assessing NAFLD histology.

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