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Oxidative Stress and Alcoholic Liver Disease
Abstract
Reactive oxygen species (ROS) are highly reactive molecules that are naturally generated in small amounts during the body's metabolic reactions and can react with and damage complex cellular molecules such as lipids, proteins, or DNA. This review describes pathways involved in ROS formation, why ROS are toxic to cells, and how the liver protects itself against ROS. Acute and chronic ethanol treatment increases the production of ROS, lowers cellular antioxidant levels, and enhances oxidative stress in many tissues, especially the liver. Ethanol-induced oxidative stress plays a major role in the mechanisms by which ethanol produces liver injury. Many pathways play a key role in how ethanol induces oxidative stress. This review summarizes some of the leading pathways and discusses the evidence for their contribution to alcohol-induced liver injury.
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“Liver diseases related to alcohol consumption are partly due to the ROS formation from ethanol (Wu and Cederbaum 2009).”
From Reactive Oxygen Species, Toxicity, Oxidative Stress, and Antioxidants: Chronic Diseases and Aging (2023) · cites this paper as Wu and Cederbaum 2009
In the citing paper
“Hepatic mitochondrial abnormalities are observed in both alcoholic fatty liver disease (AFLD) [4], [5], [6], nonalcoholic fatty liver disease (NAFLD) [7], [8], [9] and acute liver injury.”
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Impact of Embalica Officinalis: A miracle multipurpose plant
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“This is in line with earlier research showing that oxidative stress is the main cause of alcohol-related liver damage 36 .”
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Opposing Roles of CYP2E1 and ALDH2 in Binge Alcohol-Mediated Cerebellar Damage
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Pharmacological Potential of Selenoproteins in the Regulation of Oxidative Stress in Liver Diseases
Varlamova, E. G. (2026) · Pharmaceutics · doi:10.3390/pharmaceutics18091167
Metadata
- Authors
- Wu, D., & Cederbaum, A.
- Affiliations
- Icahn School of Medicine at Mount Sinai (US)
- ORCID
- Wu, Defeng
- Venue
- Seminars in Liver Disease
- Publisher
- Georg Thieme Verlag KG
- Published
- 2009-04-22
- Volume
- 29
- Issue
- 02
- Pages
- 141-154
- ISSN
- 0272-8087 (ISSN-L)
- 1098-8971
- OpenAlex
- W1981280200
- Cited by
- 342
- References
- 0
- Citations by year
- 2026: 11 · 2025: 14 · 2024: 19 · 2023: 19 · 2022: 27 · 2021: 19 · 2020: 19 · 2019: 18 · 2018: 16 · 2017: 23 · 2016: 14 · 2015: 19 · 2014: 29 · 2013: 28 · 2012: 26
- FWCI
- 15.50
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Seminars in Liver Disease (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Pathology and Forensic Medicine › Alcohol Consumption and Health Effects
- Health Sciences › Medicine › Biochemistry (medical) › Antioxidant Activity and Oxidative Stress
- Life Sciences › Pharmacology, Toxicology and Pharmaceutics › Pharmacology › Drug-Induced Hepatotoxicity and Protection
- Keywords
- oxidative stress, alcoholic liver disease, reactive oxygen species, ethanol-induced liver injury, antioxidant defense, alcohol metabolism, lipid peroxidation, DNA damage, protein oxidation
- MeSH terms
- Alcohol Drinking, Ethanol, Animals, Antioxidants, Glutathione, Humans, Iron, Kupffer Cells, Liver, Liver Diseases, Alcoholic, Mitochondria, Liver, Reactive Oxygen Species, Oxidative Stress, Cytochrome P-450 CYP2E1, Reactive Nitrogen Species
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