ArticleAlcoholism, clinical and experimental research2017
Chronic Ethanol Metabolism Inhibits Hepatic Mitochondrial Superoxide Dismutase via Lysine Acetylation.
Article in Alcoholism, clinical and experimental research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 42 citations in OpenAlex.
- The Important Role of Superoxide Dismutase 2 in Controlling Poxvirus Proliferation and Pathogenicity.Antioxidants (Basel, Switzerland) · 2026Article
- GCN5L1-Mediated Lysine Acetylation Regulates Mitochondrial Bioenergetics and Redox Homeostasis in the Aged Heart.Antioxidants (Basel, Switzerland) · 2026Article
- Molecular Networks of Redox Dysregulation in Fetal Alcohol Spectrum Disorders: Mechanisms and Therapeutic Prospects.Antioxidants (Basel, Switzerland) · 2026Review
- Metabolic biomarkers for predicting onset and severity of CAR-T therapy-induced cytokine release syndrome in multiple myeloma.Frontiers of medicine · 2025Article
- Deacetylation of SOD3 by sirtuins restores furin cleavage.Redox biochemistry and chemistry · 2025Article
- Acetylation of proximal cysteine-lysine pairs by alcohol metabolism.Redox biology · 2025Article
- Alcohol- and Low-Iron Induced Changes in Antioxidant and Energy Metabolism Associated with Protein Lys Acetylation.International journal of molecular sciences · 2024Article
- Click chemistry-based thiol redox proteomics reveals significant cysteine reduction induced by chronic ethanol consumption.Redox biology · 2023Article
- NIPSNAP1 directs dual mechanisms to restrain senescence in cancer cells.Journal of translational medicine · 2023Article
- Neuronal SIRT3 Deletion Predisposes to Female-Specific Alterations in Cellular Metabolism, Memory, and Network Excitability.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
- Effect of NaturalToxics · 2022Article
- The Brain Protein Acylation System Responds to Seizures in the Rat Model of PTZ-Induced Epilepsy.International journal of molecular sciences · 2022Article
- Alcohol-Related Liver Disease: An Overview on Pathophysiology, Diagnosis and Therapeutic Perspectives.Biomedicines · 2022Review
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- Proteomic analysis of alcohol-associated hepatitis reveals glycoprotein NMB (GPNMB) as a novel hepatic and serum biomarker.Alcohol (Fayetteville, N.Y.) · 2022Article
- Ethanol Intoxication Impairs Respiratory Function and Bacterial Clearance and Is Associated With Neutrophil Accumulation in the Lung AfterFrontiers in immunology · 2022Article
- Oxidative Stress-A Key Player in the Course of Alcohol-Related Liver Disease.Journal of clinical medicine · 2021Review
- Quantitative acetylome analysis reveals histone modifications that may predict prognosis in hepatitis B-related hepatocellular carcinoma.Clinical and translational medicine · 2021Article
- Alcohol Metabolizing Enzymes, Microsomal Ethanol Oxidizing System, Cytochrome P450 2E1, Catalase, and Aldehyde Dehydrogenase in Alcohol-Associated Liver Disease.Biomedicines · 2020Review
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundChronic ethanol (EtOH) consumption is a major cause of liver disease worldwide. Oxidative stress is a known consequence of EtOH metabolism and is thought to contribute significantly to alcoholic liver disease (ALD). Therefore, elucidating pathways leading to sustained oxidative stress and downstream redox imbalances may reveal how EtOH consumption leads to ALD. Recent studies suggest that EtOH metabolism impacts mitochondrial antioxidant processes through a number of proteomic alterations, including hyperacetylation of key antioxidant proteins.
methodsTo elucidate mechanisms of EtOH-induced hepatic oxidative stress, we investigate a role for protein hyperacetylation in modulating mitochondrial superoxide dismutase (SOD2) structure and function in a 6-week Lieber-DeCarli murine model of EtOH consumption. Our experimental approach includes immunoblotting immunohistochemistry (IHC), activity assays, mass spectrometry, and in silico modeling.
resultsWe found that EtOH metabolism significantly increased the acetylation of SOD2 at 2 functionally relevant lysine sites, K68 and K122, resulting in a 40% decrease in enzyme activity while overall SOD2 abundance was unchanged. In vitro studies also reveal which lysine residues are more susceptible to acetylation. IHC analysis demonstrates that SOD2 hyperacetylation occurs near zone 3 within the liver, which is the main EtOH-metabolizing region of the liver.
conclusionsOverall, the findings presented in this study support a role for EtOH-induced lysine acetylation as an adverse posttranslational modification within the mitochondria that directly impacts SOD2 charge state and activity. Last, the data presented here indicate that protein hyperacetylation may be a major factor contributing to an imbalance in hepatic redox homeostasis due to chronic EtOH metabolism.
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