ArticleToxicological sciences : an official journal of the Society of Toxicology2018
Alcohol Metabolism in the Progression of Human Nonalcoholic Steatohepatitis.
Article in Toxicological sciences : an official journal of the Society of Toxicology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 58 citations in OpenAlex.
- The convergent roles of metabolic dysfunction, alcohol, and iron in steatotic liver disease: a review.Bioscience reports · 2026Review
- Mitochondrial vulnerability to aldehydic load and the role mitochondrial aldehyde dehydrogenases.Pharmacological research · 2026Review
- Common human ALDH1B1 and ALDH2 variants increase neuroinflammatory response to a single ethanol dose in mice.Science advances · 2026Article
- Article
- Oxidative Stress in Liver Metabolic Dysfunction and Diseases, with a Focus on Hepatogenic Diabetes: Effect of Alcohol Consumption.Antioxidants (Basel, Switzerland) · 2025Review
- Alcohol and Metabolic Stress Synergize to Dysregulate Mitochondrial Health and Lipid Metabolism; Evidence from a Hepatocyte Spheroid Model.Function (Oxford, England) · 2025Article
- Proteomics Used in Identifying Novel Correlates of Disease in Pediatric Metabolic Dysfunction-Associated Steatotic Liver Disease.Clinical and translational science · 2025Article
- Hormone correction of dysfunctional metabolic gene expression in stem cell-derived liver tissue.Stem cell research & therapy · 2025Article
- Alcohol-Metabolizing Enzymes, Liver Diseases and Cancer.Seminars in liver disease · 2025Review
- Metabolic dysfunction-associated steatotic liver disease-induced changes in the antioxidant system: a review.Archives of toxicology · 2025Review
- A prognostic molecular signature of hepatic steatosis is spatially heterogeneous and dynamic in human liver.Cell reports. Medicine · 2024Article
- Role of gut-liver axis and glucagon-like peptide-1 receptor agonists in the treatment of metabolic dysfunction-associated fatty liver disease.World journal of gastroenterology · 2024Review
- Article
- A high-fat diet increases hepatic mitochondrial turnover through restricted acetylation in a NAFLD mouse model.American journal of physiology. Endocrinology and metabolism · 2023Article
- Breath BiopsyJournal of clinical and translational hepatology · 2023Article
- Oral Probiotic Expressing Human Ethanol Dehydrogenase Attenuates Damage Caused by Acute Alcohol Consumption in Mice.Microbiology spectrum · 2023Article
- Patients with Non-Alcoholic Fatty Liver Disease and Alcohol Dehydrogenase 1B/Aldehyde Dehydrogenase 2 Mutant Gene Have Higher Values of Serum Alanine Transaminase.Journal of personalized medicine · 2023Article
- The Concept of Cancer Stem Cells: Elaborating on ALDH1B1 as an Emerging Marker of Cancer Progression.Life (Basel, Switzerland) · 2023Review
- Daucosterol Alleviates Alcohol-Induced Hepatic Injury and Inflammation through P38/NF-κB/NLRP3 Inflammasome Pathway.Nutrients · 2023Article
- [Research progress of acetaldehyde dehydrogenase 2 in liver diseases].Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2022Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Alcohol metabolism is a well-characterized biological process that is dominated by the alcohol dehydrogenase (ADH) and aldehyde dehydrogenase (ALDH) families. Nonalcoholic steatohepatitis (NASH) is the advanced inflammatory stage of nonalcoholic fatty liver disease (NAFLD) and is known to alter the metabolism and disposition of numerous drugs. The purpose of this study was to investigate the alterations in alcohol metabolism processes in response to human NASH progression. Expression and function of ADHs, ALDHs, and catalase were examined in normal, steatosis, NASH (fatty) and NASH (not fatty) human liver samples. ALDH4A1 mRNA was significantly decreased in both NASH groups, while no significant changes were observed in the mRNA levels of other alcohol-related enzymes. The protein levels of ADH1A, ADH1B, and ADH4 were each decreased in the NASH groups, which was consistent with a decreased overall ADH activity. The protein level of ALDH2 was significantly increased in both NASH groups, while ALDH1A1 and ALDH1B1 were only decreased in NASH (fatty) samples. ALDH activity represented by oxidation of acetaldehyde was decreased in the NASH (fatty) group. The protein level of catalase was decreased in both NASH groups, though activity was unchanged. Furthermore, the significant accumulation of 4-hydroxynonenal protein adduct in NASH indicated significant oxidative stress and a potential reduction in ALDH activity. Collectively, ADH and ALDH expression and function are profoundly altered in the progression of NASH, which may have a notable impact on ADH- and ALDH-associated cellular metabolism processes and lead to significant alterations in drug metabolism mediated by these enzymes.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.