ArticleAmerican journal of physiology. Gastrointestinal and liver physiology2010
Analysis of the liver mitochondrial proteome in response to ethanol and S-adenosylmethionine treatments: novel molecular targets of disease and hepatoprotection.
Article in American journal of physiology. Gastrointestinal and liver physiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 53 citations in OpenAlex.
- Methionine Adenosyltransferase 1A and S-Adenosylmethionine in Alcohol-Associated Liver Disease.Antioxidants (Basel, Switzerland) · 2025Review
- Targeting mitochondrial transporters and metabolic reprogramming for disease treatment.Journal of translational medicine · 2025Review
- Comprehensive review on alcohol-induced protein modifications in hepatic mitochondrial membranes and their functional implications.Molecular biology reports · 2025Review
- Prolonged Intestinal Ethanol Absorption and Oxidative Stress: Revisiting the Gut-Liver Axis in Alcohol-Associated Disease.International journal of molecular sciences · 2025Review
- Anti-Inflammatory Drugs for Alcoholic Liver Disease: A Systematic Review on Survival and Adverse Events.International journal of hepatology · 2025Review
- Acute and chronic blood serum proteome changes in patients with methanol poisoning.Scientific reports · 2022Article
- Primary Biliary Cholangitis and Primary Sclerosing Cholangitis: Current Knowledge of Pathogenesis and Therapeutics.Biomedicines · 2022Review
- Structure-activity features of purines and their receptors: implications in cell physiopathology.Molecular biomedicine · 2022Review
- Oxidative stress in alcohol-related liver disease.World journal of hepatology · 2020Review
- Article
- Hepatic Mitochondrial Defects in a Nonalcoholic Fatty Liver Disease Mouse Model Are Associated with Increased Degradation of Oxidative Phosphorylation Subunits.Molecular & cellular proteomics : MCP · 2018Article
- Article
- The methyl donor S-adenosylmethionine prevents liver hypoxia and dysregulation of mitochondrial bioenergetic function in a rat model of alcohol-induced fatty liver disease.Redox biology · 2016Article
- The Molecular Circadian Clock and Alcohol-Induced Liver Injury.Biomolecules · 2015Review
- Changes of the Cytoplasmic Proteome in Response to Alcoholic Hepatotoxicity in Rats.International journal of molecular sciences · 2015Article
- Molecular mechanisms for alcoholic hepatitis based on analysis of gene expression profile.Hepatitis monthly · 2015Article
- Nutritional models of foetal programming and nutrigenomic and epigenomic dysregulations of fatty acid metabolism in the liver and heart.Pflugers Archiv : European journal of physiology · 2014Review
- Involvement of the mitochondrial permeability transition pore in chronic ethanol-mediated liver injury in mice.American journal of physiology. Gastrointestinal and liver physiology · 2014Article
- Mitochondrial dysfunction and tissue injury by alcohol, high fat, nonalcoholic substances and pathological conditions through post-translational protein modifications.Redox biology · 2014Review
- Acute ethanol causes hepatic mitochondrial depolarization in mice: role of ethanol metabolism.PloS one · 2014Article
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9 authors at 1 institution in 1 country.
Funding
Abstract
S-adenosylmethionine (SAM) minimizes alcohol hepatotoxicity; however, the molecular mechanisms responsible for SAM hepatoprotection remain unknown. Herein, we use proteomics to determine whether the hepatoprotective action of SAM against early-stage alcoholic liver disease is linked to alterations in the mitochondrial proteome. For this, male rats were fed control or ethanol-containing liquid diets +/- SAM and liver mitochondria were prepared for proteomic analysis. Two-dimensional isoelectric focusing (2D IEF/SDS-PAGE) and blue native gel electrophoresis (BN-PAGE) were used to determine changes in matrix and oxidative phosphorylation (OxPhos) proteins, respectively. SAM coadministration minimized alcohol-dependent inflammation and preserved mitochondrial respiration. SAM supplementation preserved liver SAM levels in ethanol-fed rats; however, mitochondrial SAM levels were increased by ethanol and SAM treatments. With use of 2D IEF/SDS-PAGE, 30 proteins showed significant changes in abundance in response to ethanol, SAM, or both. Classes of proteins affected by ethanol and SAM treatments were chaperones, beta oxidation proteins, sulfur metabolism proteins, and dehydrogenase enzymes involved in methionine, glycine, and choline metabolism. BN-PAGE revealed novel changes in the levels of 19 OxPhos proteins in response to ethanol, SAM, or both. Ethanol- and SAM-dependent alterations in the proteome were not linked to corresponding changes in gene expression. In conclusion, ethanol and SAM treatment led to multiple changes in the liver mitochondrial proteome. The protective effects of SAM against alcohol toxicity are mediated, in part, through maintenance of proteins involved in key mitochondrial energy conserving and biosynthetic pathways. This study demonstrates that SAM may be a promising candidate for treatment of alcoholic liver disease.
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