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

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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: closed (10 April 2026) | Viewed by 19183

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Dr. Marco Fiore

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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
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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

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Keywords

alcohol
alcohol use disorder
reactive oxygen species
antioxidant defense

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Published Papers (10 papers)

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Research

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24 pages, 4062 KB

Open AccessArticle

Role of L-Arginine in the Gut–Liver Axis of Female Mice: Mediating Ethanol’s Alterations in Hepatic Steatosis and Oxidative Stress

by Kaitlyn Daff, Yingchun Han, Zhuoying Feng, Mala Upadhyay, Vyshnavi Sivampeta, Abirami Rajasekaran, Naseer Sangwan and Gail A. M. Cresci

Antioxidants 2026, 15(5), 537; https://doi.org/10.3390/antiox15050537 - 24 Apr 2026

Viewed by 444

Abstract

Ethanol exposure causes microbial imbalance, damages the gut barrier, and increases oxidative stress along the gut–liver axis, leading to the development and progression of alcohol-associated liver disease (ALD). Arginine is a conditionally essential amino acid that may play a key role in maintaining redox homeostasis and mediating host–microbiota crosstalk. We hypothesized that supplemental arginine provided during chronic ethanol exposure in mice would mitigate oxidative damage via the gut–liver axis. Our findings suggest that arginine supplementation mediated hepatic steatosis, preserved body weight and fat, and reduced oxidative stress in the gut–liver axis. These changes were associated with alterations in gut microbiota composition and function. These data support a potential role for arginine supplementation in mitigating ethanol-induced oxidative damage via the gut–liver axis. Full article

(This article belongs to the Special Issue Alcohol-Induced Oxidative Stress in Health and Disease, 2nd Edition)

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34 pages, 2919 KB

Open AccessArticle

Alcohol Consumption and DNA Methylation in a Mediterranean Cohort: A Focus on Oxidative Stress and Aging Biomarkers

by Oscar Coltell, Eva M. Asensio, José V. Sorlí, Rebeca Fernández-Carrión, Carolina Ortega-Azorín, Rocío Barragán, Alejandro Perez-Fidalgo, Olga Portolés, Jose M. Ordovas and Dolores Corella

Antioxidants 2026, 15(2), 197; https://doi.org/10.3390/antiox15020197 - 2 Feb 2026

Viewed by 1336

Abstract

There is considerable interest in the connection between alcohol-induced oxidative stress, DNA methylation, antioxidants, and accelerated aging across diverse populations. Nevertheless, self-reported alcohol consumption is prone to bias, and objective biomarkers of alcohol intake are needed. Our aims were to investigate the performance of an epigenomic biomarker of alcohol consumption in a Mediterranean population using self-reported data and the biomarker gamma-glutamyl transferase (GGT); to examine the effects of alcohol (self-reported and biomarker-assessed) on epigenome-wide methylation; to analyze the association between alcohol (self-reported and biomarker-assessed) and telomere length and other aging biomarkers; and to explore the modulating effect of the Mediterranean diet (MedDiet). We performed blood epigenome-wide methylation studies (EWAS) in a Mediterranean cohort (aged 55–75 years). Self-reported alcohol consumption and MedDiet were assessed by questionnaires. A replication cohort (cohort 2) from the same area was also analyzed. For both cohorts, the DNA methylation-based biomarker (450-CpGs) was computed alongside epigenetic clocks for the following biological age acceleration metrics: DNAm telomere length, GrimAgeAcceleration, PhenoAgeAcceleration, and CausalityAgeYing (cohort 1). The association between the epigenomic biomarker and self-reported alcohol consumption was significant (p < 0.001) in both cohorts, but modest. However, the association was stronger when predicting high alcohol intake (AUC: 0.76; 95%CI: 0.65–0.86; p < 0.0001). In the EWAS, the hit (cg06690548-SLC7A11, in a cystine transporter that enhances glutathione production for antioxidant defense) was shared among the self-reported alcohol consumption, GGT, and the epigenomic biomarker, with alcohol linked to hypomethylation. We detected differential methylation in pre-selected oxidative stress-related genes. Enrichment analysis revealed “Rap1 signaling pathway” as the hit (p < 0.00001). High self-reported alcohol consumption and the epigenomic biomarker were associated with shorter telomere length (p < 0.05) in cohort 1. Additionally, a modulation by Mediterranean diet adherence was hypothesized. No significant associations were found between self-reported alcohol intake and the other aging biomarkers; however, the epigenomic score was directly associated with GrimAge, PhenoAge and CausAgeYing biomarkers in cohort 1 (p < 0.001), and two were replicated in cohort 2. In conclusion, alcohol intake has an impact on DNA methylation at the epigenome-wide level in this Mediterranean population, replicating the main hits from other populations and validating the epigenomic biomarker for intake, although improvement is needed. Moreover, several associations with aging biomarkers were observed. Full article

(This article belongs to the Special Issue Alcohol-Induced Oxidative Stress in Health and Disease, 2nd Edition)

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23 pages, 1267 KB

Open AccessArticle

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

Cited by 1 | Viewed by 1726

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 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

Open AccessArticle

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 7 | Viewed by 2782

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 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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22 pages, 1012 KB

Open AccessReview

Oxidative Stress and Alcohol-Related Hepatitis: A Role for Future Therapies

by Francesca D’Arcangelo, Neil Rajoriya and Patricia F. Lalor

Antioxidants 2026, 15(4), 493; https://doi.org/10.3390/antiox15040493 - 16 Apr 2026

Viewed by 738

Abstract

Alcohol-associated Hepatitis (AH) is a rare acute injury caused by alcohol consumption, which can lead to one of the most severe manifestations of liver disease. It is part of the alcohol-related liver diseases (ArLD) spectrum, which represents a major global health burden, with oxidative stress and inflammation serving as central, interconnected pathogenic mechanisms. Chronic alcohol (ethanol) consumption induces hepatic reactive oxygen species (ROS) generation through multiple pathways, including cytochrome P450 2E1 (CYP2E1) induction, mitochondrial dysfunction, and NADPH oxidase activation. These oxidative insults trigger a cascade of cellular damage encompassing lipid peroxidation, protein adduct formation, DNA damage, and endoplasmic reticulum stress, ultimately leading to hepatocyte dysfunction and multiple forms of cell death, including apoptosis, necroptosis, pyroptosis, and ferroptosis. The inflammatory response, orchestrated primarily by Kupffer cells and infiltrating neutrophils through Toll-like receptor (TLR) signalling and inflammasome activation, not only amplifies hepatic injury but also promotes fibrogenesis through hepatic stellate cell activation. Neutrophils, characterised by elevated lipocalin-2 expression and spontaneous NETosis in AH, exhibit a paradoxical role by driving both tissue damage and repair. Current therapeutic strategies include corticosteroids, which remain the first-line treatment for severe AH, while emerging therapies targeting the gut–liver axis, hepatic regeneration, and specific molecular targets show promise in clinical trials. This review comprehensively examines the molecular crosstalk between oxidative stress and inflammation in the pathogenesis of AH to highlight current and investigational therapeutic approaches targeting these interconnected pathways. Full article

(This article belongs to the Special Issue Alcohol-Induced Oxidative Stress in Health and Disease, 2nd Edition)

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33 pages, 3614 KB

Open AccessReview

Molecular Networks of Redox Dysregulation in Fetal Alcohol Spectrum Disorders: Mechanisms and Therapeutic Prospects

by Xiaoqing Wang and Shao-Yu Chen

Antioxidants 2026, 15(4), 470; https://doi.org/10.3390/antiox15040470 - 10 Apr 2026

Viewed by 842

Abstract

Fetal alcohol spectrum disorders (FASD) encompass a continuum of developmental abnormalities caused by prenatal alcohol exposure, resulting in persistent neurodevelopmental and structural defects. Accumulating evidence indicates that redox dysregulation plays a central role in the pathogenesis of FASD. Ethanol disrupts cellular redox homeostasis by promoting excessive reactive oxygen species production and depleting endogenous antioxidants, thereby perturbing key redox-sensitive molecular networks. Dysregulation of these pathways leads to mitochondrial dysfunction, endoplasmic reticulum stress, lysosome dysfunction, and disrupted cellular processes, including proliferation, differentiation, and migration, while also promoting apoptosis and neuroinflammation, ultimately leading to the developmental abnormalities characteristic of FASD. Recent studies demonstrate that antioxidant supplementation or targeted modulation of redox-sensitive signaling can mitigate these deleterious effects in preclinical models. This review synthesizes current knowledge of the molecular networks underlying redox dysregulation in FASD and discusses emerging antioxidant and dietary interventions with therapeutic potential. Elucidating these mechanisms provides critical insight into the pathogenesis of FASD and may inform the development of effective strategies for the prevention and treatment of FASD. Full article

(This article belongs to the Special Issue Alcohol-Induced Oxidative Stress in Health and Disease, 2nd Edition)

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35 pages, 3230 KB

Open AccessReview

Timeless and Stainless Alcohol: Concentric Waves from Its Oxidative Metabolism and Related Oxidative Stress

by Riccardo Maccioni, Simone Tambaro, Laura Doro, Valentina Bassareo, Alessandra T. Peana and Elio Acquas

Antioxidants 2026, 15(2), 216; https://doi.org/10.3390/antiox15020216 - 6 Feb 2026

Cited by 1 | Viewed by 1301

Abstract

Alcohol is a molecule whose multiple effects in living organisms exemplify how profound biological complexity can arise from an exceptionally simple chemical structure interacting with the cellular biochemical machinery. This review was conceived to provide an up-to-date synthesis of the current knowledge on the multifaceted consequences of alcohol oxidative metabolism and alcohol-derived oxidative stress, ranging from disruption of subcellular and cellular homeostasis to impairment of organ function. This study primarily focuses on the consequences of alcohol metabolism and on the mechanisms by which the rise of its main metabolite, acetaldehyde, and of reactive oxygen species (ROS), generates oxidative stress by-products and molecular adducts responsible for compromising cellular energy balance and antioxidant defense mechanisms. In particular, this review aims to provide an exhaustive representation of the mechanisms, causes, and consequences of alcohol oxidative metabolism: this is accomplished by taking into account alcohol-induced modifications of gene expression of cellular antioxidant determinants, the role of epigenetic mechanisms, and that of gene polymorphisms linked to alcohol-dependent oxidative stress and responsible for serious diseases such as, among others, alcoholic hepatitis, cirrhosis, and hepatocellular carcinoma. In addition, this review highlights the role of alcohol oxidative metabolism in the brain, which, in the acute setting, activates the dopaminergic system mainly involved in alcohol reinforcing properties and, upon chronic exposure, contributes to neurodegenerative disorders. Finally, a dedicated paragraph explores autophagy as an integrative mechanism underlying the effects of alcohol-related oxidative stress across multiple organs, including the liver, heart, and brain. Full article

(This article belongs to the Special Issue Alcohol-Induced Oxidative Stress in Health and Disease, 2nd Edition)

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27 pages, 1586 KB

Open AccessReview

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

Cited by 3 | Viewed by 1857

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 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

Open AccessReview

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

Cited by 2 | Viewed by 2186

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 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

Open AccessReview

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

Cited by 7 | Viewed by 4346

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 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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