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Antioxidants
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Alcohol-Induced Oxidative Stress in Health and Disease, 2nd Edition
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Alcohol-Induced Oxidative Stress in Health and Disease, 2nd Edition

A special issue of Antioxidants (ISSN 2076-3921). This special issue belongs to the section "Health Outcomes of Antioxidants and Oxidative Stress".

Deadline for manuscript submissions: 10 April 2026 | Viewed by 6858

Special Issue Editor

Dr. Marco Fiore

E-Mail Website
Guest Editor
Institute of Biochemistry and Cell Biology (IBBC), National Research Council (CNR), Department of Sense Organs, University Sapienza of Rome, Viale del Policlinico, 155 Rome, Italy
Interests: neurobiology; endocrinology; neurotrophins; oxidative stress; cancer; toxicology; addiction; antioxidants; polyphenols; alcohol use disorders
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Alcohol is one of the oldest and most common recreational substances and is present in various beverages such as wine, beer, and spirits. While moderate alcohol consumption may elicit pleasure, euphoria, increased sociability, and decreased anxiety, it also carries a wide range of short-term and long-term adverse effects. These include neurocognitive impairment, nausea, vomiting, dizziness, and hangover symptoms. Chronic alcohol abuse leads to alcohol use disorder, addiction, and withdrawal, all of which severely impact health, causing liver and brain damage, and significantly increasing the risk of cancer. A key mechanism underlying these detrimental effects is alcohol-induced oxidative stress.

Alcohol metabolism, through both mitochondrial and microsomal pathways, generates reactive oxygen species (ROS) and reactive nitrogen species (RNS), overwhelming the body's endogenous antioxidant defense system. This oxidative stress results in cellular and tissue damage, disrupting biological functions and leading to severe health consequences. Research suggests that antioxidants may mitigate some of these harmful effects, offering a potential therapeutic approach.

Building on the fruitful first edition of this Special Issue, available at https://www.mdpi.com/si/139960, the second edition continues to explore the complexities of alcohol-induced oxidative stress and its implications for health and disease. We invite original research and review articles that delve into clinical and preclinical data, providing insights into this critical area of study and guiding future research directions.

Dr. Marco Fiore
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 250 words) can be sent to the Editorial Office for assessment.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Antioxidants is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2900 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • alcohol
  • alcohol use disorder
  • reactive oxygen species
  • antioxidant defense

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Published Papers (5 papers)

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Research

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23 pages, 1267 KB  
Article
Dysregulated Expression of Canonical and Non-Canonical Glycolytic Enzyme Isoforms in Peripheral Blood from Subjects with Alcohol Use Disorder and from Individuals with Acute Alcohol Consumption
by Maura Rojas-Pirela, Daniel Salete-Granado, Diego Andrade-Alviárez, Alejandro Prieto-Rojas, Cristina Rodríguez, María-Lourdes Aguilar-Sánchez, David Puertas-Miranda, María-Ángeles Pérez-Nieto, Vanessa Rueda-Cala, Candy Pérez, Wilfredo Quiñones, Paul A. M. Michels, Ángeles Almeida and Miguel Marcos
Antioxidants 2025, 14(9), 1143; https://doi.org/10.3390/antiox14091143 - 22 Sep 2025
Viewed by 897
Abstract
Glycolysis is primarily involved in ATP production but also modulates oxidative stress. Chronic alcohol consumption is correlated with an increased incidence of multiple diseases, including cancer and neurodegenerative diseases (NDDs), though the underlying mechanisms remain unclear. Guided by a literature review and bioinformatics [...] Read more.
Glycolysis is primarily involved in ATP production but also modulates oxidative stress. Chronic alcohol consumption is correlated with an increased incidence of multiple diseases, including cancer and neurodegenerative diseases (NDDs), though the underlying mechanisms remain unclear. Guided by a literature review and bioinformatics analysis, we evaluated the expression of 22 genes encoding various isoforms of seven glycolytic enzymes (GEs) in the peripheral blood of patients with alcohol use disorder (AUD), individuals with acute alcohol consumption (AAC), and their respective control groups using qPCR. In parallel, we evaluated the expression of selected genes coding for GEs linked to NDDs, as well as astrocytic markers in primary mouse astrocyte cultures exposed to ethanol. Thirteen GE-related genes, including non-canonical isoforms, were significantly dysregulated in AUD patients; notably, eight of these genes showed similar alterations in individuals with AAC. Several enzymes encoded by these genes are known to be regulated by oxidative stress. Ethanol-exposed astrocytes also showed altered expression of glycolytic genes associated with NDDs and astrocyte function. These findings indicate that glycolytic dysregulation is driven by ethanol intake, regardless of exposure duration or organic damage, highlighting a link between ethanol-driven redox imbalance and glycolytic remodeling, which could contribute to organ damage. Full article
(This article belongs to the Special Issue Alcohol-Induced Oxidative Stress in Health and Disease, 2nd Edition)
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18 pages, 3245 KB  
Article
Weizmannia coagulans BC99 Attenuates Oxidative Stress Induced by Acute Alcoholic Liver Injury via Nrf2/SKN-1 Pathway and Liver Metabolism Regulation
by Ying Wu, Cheng Li, Yinyin Gao, Jie Zhang, Yao Dong, Lina Zhao, Yuwan Li and Shaobin Gu
Antioxidants 2025, 14(1), 117; https://doi.org/10.3390/antiox14010117 - 20 Jan 2025
Cited by 4 | Viewed by 2110
Abstract
Acute alcoholic liver injury (AALI) remains a significant global health concern, primarily driven by oxidative stress. This study investigated the protective mechanisms of Weizmannia coagulans BC99 against alcohol-induced oxidative stress using a dual model in rats and Caenorhabditis elegans. In rats, excessive alcohol [...] Read more.
Acute alcoholic liver injury (AALI) remains a significant global health concern, primarily driven by oxidative stress. This study investigated the protective mechanisms of Weizmannia coagulans BC99 against alcohol-induced oxidative stress using a dual model in rats and Caenorhabditis elegans. In rats, excessive alcohol was predominantly metabolized via the CYP2E1 pathway, leading to severe oxidative stress. However, intervention with BC99 suppressed CYP2E1 expression and enhanced antioxidant enzyme activities through the Nrf2/SKN-1 pathway, thereby alleviating oxidative stress. Additionally, BC99 treatment elevated glutamate and aspartate levels while reducing glycerate and glucose, which collectively increased glutathione levels and mitigated oxidative stress triggered by glucose metabolism disorders. In C. elegans, BC99 reduced excessive ROS by upregulating Nrf2/skn-1, daf-16, and their downstream antioxidant genes, consequently alleviating the biotoxicity associated with alcohol-induced oxidative damage. The protective effects of BC99 were markedly diminished in the skn-1 mutant (GR2245) and daf-16 mutant (CF1038), further confirming the pivotal roles of SKN-1 and DAF-16 pathways in BC99-mediated antioxidant protection. Taken together, these findings reveal that BC99 mitigates alcohol-induced oxidative stress by activating the Nrf2/SKN-1 pathway and regulating liver metabolites to eliminate excess ROS, thereby providing a theoretical basis for the application of probiotics in preventing acute alcoholic liver injury. Full article
(This article belongs to the Special Issue Alcohol-Induced Oxidative Stress in Health and Disease, 2nd Edition)
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Review

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27 pages, 1586 KB  
Review
Oxidative Stress in Liver Metabolic Dysfunction and Diseases, with a Focus on Hepatogenic Diabetes: Effect of Alcohol Consumption
by Martha Lucinda Contreras-Zentella, Lorena Carmina Hernández-Espinosa and Rolando Hernández-Muñoz
Antioxidants 2025, 14(12), 1494; https://doi.org/10.3390/antiox14121494 - 12 Dec 2025
Viewed by 333
Abstract
Metabolic dysfunction–associated fatty liver disease (MASLD) is associated with severe forms of liver injury, including fibrosis and cirrhosis. The main risk factors for MASLD—obesity, type 2 diabetes mellitus (T2DM), dyslipidemia, and insulin resistance (IR)—contribute to metabolic disturbances that initiate hepatic steatosis. Metabolic and [...] Read more.
Metabolic dysfunction–associated fatty liver disease (MASLD) is associated with severe forms of liver injury, including fibrosis and cirrhosis. The main risk factors for MASLD—obesity, type 2 diabetes mellitus (T2DM), dyslipidemia, and insulin resistance (IR)—contribute to metabolic disturbances that initiate hepatic steatosis. Metabolic and alcohol-related liver disease (MetALD) describes patients with MASLD who also present alcohol-associated hepatic injury. Chronic oxidative and inflammatory stress promotes the progression of steatosis in both conditions. T2DM and chronic alcohol consumption are independent lifestyle-related risk factors for cirrhosis within the spectrum of metabolic dysfunction–related liver disease (MASLD and MetALD). The coexistence of both conditions may exacerbate hepatic pathological alterations. IR, which is frequently observed in patients with cirrhosis, can lead to the development of a condition known as hepatogenic diabetes (HD). HD is characterized by hyperinsulinemia, IR, and β-cell dysfunction occurring during the onset of cirrhosis and is associated with hepatic inflammation even in the absence of traditional metabolic risk factors such as obesity or a prior history of T2DM. In this context, alcohol intake enhances lipolysis in peripheral tissues, promotes hepatic steatosis, and aggravates metabolic dysfunction, ultimately contributing to excessive mitochondrial production of reactive oxygen species (ROS). Therefore, the present review examines the role of oxidative stress—both alcohol-related and non-alcohol–related—in the pathogenesis of HD, with particular emphasis on ethanol metabolism, oxidative stress, and their interactions in conditions such as T2DM and MetALD. Full article
(This article belongs to the Special Issue Alcohol-Induced Oxidative Stress in Health and Disease, 2nd Edition)
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29 pages, 2185 KB  
Review
Methionine Adenosyltransferase 1A and S-Adenosylmethionine in Alcohol-Associated Liver Disease
by Lucía Barbier-Torres, Jyoti Chhimwal, José M. Mato and Shelly C. Lu
Antioxidants 2025, 14(12), 1486; https://doi.org/10.3390/antiox14121486 - 11 Dec 2025
Viewed by 225
Abstract
Alcohol-associated liver disease (ALD) is a leading cause of liver-related morbidity, mortality, and premature death worldwide. Its pathogenesis is complex and incompletely understood, with disrupted methionine metabolism as a key contributor. This pathway converts methionine into S-adenosylmethionine (SAM or SAMe), the principal methyl [...] Read more.
Alcohol-associated liver disease (ALD) is a leading cause of liver-related morbidity, mortality, and premature death worldwide. Its pathogenesis is complex and incompletely understood, with disrupted methionine metabolism as a key contributor. This pathway converts methionine into S-adenosylmethionine (SAM or SAMe), the principal methyl donor, a precursor of glutathione (GSH), and a critical regulator of hepatocellular function. Alterations in methionine metabolism are primarily driven by downregulation of methionine adenosyltransferase 1A (MAT1A), the liver-specific gene encoding the MATα1 subunit responsible for SAMe biosynthesis. Reduced MAT1A expression and activity lead to hepatic SAMe and GSH deficiency, resulting in global hypomethylation, mitochondrial dysfunction, impaired lipid metabolism, and progressive liver injury, hallmarks of ALD. Recent studies show that MATα1 also localizes to hepatocyte mitochondria, where its selective depletion contributes to mitochondrial dysfunction in ALD. Experimental models demonstrate that SAMe supplementation restores methylation capacity, replenishes GSH, reduces oxidative stress, and improves mitochondrial function and liver histology. Preservation of mitochondrial MATα1 also protects against ALD, underscoring its importance in hepatocellular health. Clinical exploration of SAMe in early-stage ALD suggests potential benefit and motivates continued investigation into treatment strategies that build on and extend beyond supplementation. This review summarizes current knowledge on the role of the MAT1A/SAMe axis in ALD pathophysiology, emphasizing molecular functions and critically evaluating preclinical and clinical evidence for potential therapy. Full article
(This article belongs to the Special Issue Alcohol-Induced Oxidative Stress in Health and Disease, 2nd Edition)
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16 pages, 629 KB  
Review
Alcohol-Induced Oxidative Stress and Gut–Liver–Brain Crosstalk: Expanding the Paradigm from ALD to MetALD
by Jeong-Yoon Lee, Young-Min Jee, Keungmo Yang and Tom Ryu
Antioxidants 2025, 14(10), 1196; https://doi.org/10.3390/antiox14101196 - 1 Oct 2025
Viewed by 2236
Abstract
Alcohol-associated liver disease (ALD) includes a spectrum from steatosis and steatohepatitis to cirrhosis and hepatocellular carcinoma driven by oxidative stress, immune activation, and systemic inflammation. Ethanol metabolism through alcohol dehydrogenase, aldehyde dehydrogenase, and cytochrome P450 2E1 generates reactive oxygen and nitrogen species, leading [...] Read more.
Alcohol-associated liver disease (ALD) includes a spectrum from steatosis and steatohepatitis to cirrhosis and hepatocellular carcinoma driven by oxidative stress, immune activation, and systemic inflammation. Ethanol metabolism through alcohol dehydrogenase, aldehyde dehydrogenase, and cytochrome P450 2E1 generates reactive oxygen and nitrogen species, leading to mitochondrial dysfunction, hepatocellular injury, and activation of inflammatory and fibrogenic pathways. Beyond hepatic effects, ALD engages the gut–liver–brain axis, where microbial dysbiosis, blood–brain barrier disruption, and neuroinflammation contribute to cognitive impairment and cerebrovascular risk. The emerging concept, metabolic dysfunction-associated steatotic liver disease and increased alcohol intake (MetALD), presents the synergistic impact of alcohol and metabolic comorbidities, enhancing oxidative injury and fibrosis. This review summarizes key mechanisms connecting oxidative stress to multisystem pathology and highlights the need for precision therapies targeting redox imbalance, immune dysregulation, and gut–brain–liver interactions to improve outcomes in ALD and MetALD. Full article
(This article belongs to the Special Issue Alcohol-Induced Oxidative Stress in Health and Disease, 2nd Edition)
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