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3 pages, 156 KiB

Open AccessEditorial

Oxidative Stress in Alcohol Abuse: An Unfortunately Still Open Question

by Marco Fiore

Antioxidants 2024, 13(8), 934; https://doi.org/10.3390/antiox13080934 - 1 Aug 2024

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Abstract

As the guest editor of this Special Issue “Alcohol-Induced Oxidative Stress in Health and Disease” of Antioxidants (https://www [...] Full article

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

Research

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19 pages, 33834 KiB

Open AccessArticle

Alcohol Triggers the Accumulation of Oxidatively Damaged Proteins in Neuronal Cells and Tissues

by Anusha W. Mudyanselage, Buddhika C. Wijamunige, Artur Kocoń, Ricky Turner, Denise McLean, Benito Morentin, Luis F. Callado and Wayne G. Carter

Antioxidants 2024, 13(5), 580; https://doi.org/10.3390/antiox13050580 - 8 May 2024

Viewed by 4614

Abstract

Alcohol is toxic to neurons and can trigger alcohol-related brain damage, neuronal loss, and cognitive decline. Neuronal cells may be vulnerable to alcohol toxicity and damage from oxidative stress after differentiation. To consider this further, the toxicity of alcohol to undifferentiated SH-SY5Y cells [...] Read more.

Alcohol is toxic to neurons and can trigger alcohol-related brain damage, neuronal loss, and cognitive decline. Neuronal cells may be vulnerable to alcohol toxicity and damage from oxidative stress after differentiation. To consider this further, the toxicity of alcohol to undifferentiated SH-SY5Y cells was compared with that of cells that had been acutely differentiated. Cells were exposed to alcohol over a concentration range of 0–200 mM for up to 24 h and alcohol effects on cell viability were evaluated via MTT and LDH assays. Effects on mitochondrial morphology were examined via transmission electron microscopy, and mitochondrial functionality was examined using measurements of ATP and the production of reactive oxygen species (ROS). Alcohol reduced cell viability and depleted ATP levels in a concentration- and exposure duration-dependent manner, with undifferentiated cells more vulnerable to toxicity. Alcohol exposure resulted in neurite retraction, altered mitochondrial morphology, and increased the levels of ROS in proportion to alcohol concentration; these peaked after 3 and 6 h exposures and were significantly higher in differentiated cells. Protein carbonyl content (PCC) lagged behind ROS production and peaked after 12 and 24 h, increasing in proportion to alcohol concentration, with higher levels in differentiated cells. Carbonylated proteins were characterised by their denatured molecular weights and overlapped with those from adult post-mortem brain tissue, with levels of PCC higher in alcoholic subjects than matched controls. Hence, alcohol can potentially trigger cell and tissue damage from oxidative stress and the accumulation of oxidatively damaged proteins. Full article

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

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19 pages, 4353 KiB

Open AccessArticle

Tributyrin Supplementation Rescues Chronic–Binge Ethanol-Induced Oxidative Stress in the Gut–Lung Axis in Mice

by Anthony Santilli, David Shapiro, Yingchun Han, Naseer Sangwan and Gail A. M. Cresci

Antioxidants 2024, 13(4), 472; https://doi.org/10.3390/antiox13040472 - 17 Apr 2024

Cited by 2 | Viewed by 2090

Abstract

Excessive alcohol consumption increases the severity and worsens outcomes of pulmonary infections, often due to oxidative stress and tissue damage. While the mechanism behind this relationship is multifaceted, recent evidence suggests ethanol-induced changes to the gut microbiome impact the gut–lung axis. To assess [...] Read more.

Excessive alcohol consumption increases the severity and worsens outcomes of pulmonary infections, often due to oxidative stress and tissue damage. While the mechanism behind this relationship is multifaceted, recent evidence suggests ethanol-induced changes to the gut microbiome impact the gut–lung axis. To assess this, a chronic–binge ethanol feeding mouse model was used to determine how ethanol altered the gut microbiome, small intestinal epithelial barrier, and immune responses, as well as neutrophil abundance and oxidative stress in the lungs, and how supporting gut health with tributyrin supplementation during chronic–binge ethanol exposure affected these responses. We found that ethanol consumption altered gut bacterial taxa and metabolic processes, distorted small intestinal immune responses, and induced both bacteria and endotoxin translocation into the lymphatic and circulatory systems. These changes were associated with increased neutrophil (Ly6G) presence and markers of oxidative stress, lipocalin-2 and myeloperoxidase, in the lungs. Importantly, tributyrin supplementation during ethanol exposure rescued gut bacterial function (p < 0.05), small intestinal barrier integrity, and immune responses, as well as reducing both Ly6G mRNA (p < 0.05) and lipocalin-2 mRNA (p < 0.01) in the lungs. These data suggest ethanol-associated disruption of gut homeostasis influenced the health of the lungs, and that therapeutics supporting gut health may also support lung health. Full article

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

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19 pages, 6179 KiB

Open AccessArticle

Nucleoredoxin Redox Interactions Are Sensitized by Aging and Potentiated by Chronic Alcohol Consumption in the Mouse Liver

by Osiris Germán Idelfonso-García, Brisa Rodope Alarcón-Sánchez, Dafne Guerrero-Escalera, Norma Arely López-Hernández, José Luis Pérez-Hernández, Ruth Pacheco-Rivera, Jesús Serrano-Luna, Osbaldo Resendis-Antonio, Erick Andrés Muciño-Olmos, Diana Ivette Aparicio-Bautista, Gustavo Basurto-Islas, Rafael Baltiérrez-Hoyos, Verónica Rocío Vásquez-Garzón, Saúl Villa-Treviño, Pablo Muriel, Héctor Serrano, Julio Isael Pérez-Carreón and Jaime Arellanes-Robledo

Antioxidants 2024, 13(3), 257; https://doi.org/10.3390/antiox13030257 - 20 Feb 2024

Viewed by 2391

Abstract

Aging is characterized by increased reactive species, leading to redox imbalance, oxidative damage, and senescence. The adverse effects of alcohol consumption potentiate aging-associated alterations, promoting several diseases, including liver diseases. Nucleoredoxin (NXN) is a redox-sensitive enzyme that targets reactive oxygen species and regulates [...] Read more.

Aging is characterized by increased reactive species, leading to redox imbalance, oxidative damage, and senescence. The adverse effects of alcohol consumption potentiate aging-associated alterations, promoting several diseases, including liver diseases. Nucleoredoxin (NXN) is a redox-sensitive enzyme that targets reactive oxygen species and regulates key cellular processes through redox protein–protein interactions. Here, we determine the effect of chronic alcohol consumption on NXN-dependent redox interactions in the liver of aged mice. We found that chronic alcohol consumption preferentially promotes the localization of NXN either into or alongside senescent cells, declines its interacting capability, and worsens the altered interaction ratio of NXN with FLII, MYD88, CAMK2A, and PFK1 proteins induced by aging. In addition, carbonylated protein and cell proliferation increased, and the ratios of collagen I and collagen III were inverted. Thus, we demonstrate an emerging phenomenon associated with altered redox homeostasis during aging, as shown by the declining capability of NXN to interact with partner proteins, which is enhanced by chronic alcohol consumption in the mouse liver. This evidence opens an attractive window to elucidate the consequences of both aging and chronic alcohol consumption on the downstream signaling pathways regulated by NXN-dependent redox-sensitive interactions. Full article

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

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18 pages, 3816 KiB

Open AccessArticle

Liposomal Glutathione Augments Immune Defenses against Respiratory Syncytial Virus in Neonatal Mice Exposed in Utero to Ethanol

by Theresa W. Gauthier, Xiao-Du Ping, Frank L. Harris and Lou Ann S. Brown

Antioxidants 2024, 13(2), 137; https://doi.org/10.3390/antiox13020137 - 23 Jan 2024

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Abstract

We previously reported that maternal alcohol use increased the risk of sepsis in premature and term newborns. In the neonatal mouse, fetal ethanol (ETOH) exposure depleted the antioxidant glutathione (GSH), which promoted alveolar macrophage (AM) immunosuppression and respiratory syncytial virus (RSV) infections. In [...] Read more.

We previously reported that maternal alcohol use increased the risk of sepsis in premature and term newborns. In the neonatal mouse, fetal ethanol (ETOH) exposure depleted the antioxidant glutathione (GSH), which promoted alveolar macrophage (AM) immunosuppression and respiratory syncytial virus (RSV) infections. In this study, we explored if oral liposomal GSH (LGSH) would attenuate oxidant stress and RSV infections in the ETOH-exposed mouse pups. C57BL/6 female mice were pair-fed a liquid diet with 25% of calories from ethanol or maltose–dextrin. Postnatal day 10 pups were randomized to intranasal saline, LGSH, and RSV. After 48 h, we assessed oxidant stress, AM immunosuppression, pulmonary RSV burden, and acute lung injury. Fetal ETOH exposure increased oxidant stress threefold, lung RSV burden twofold and acute lung injury threefold. AMs were immunosuppressed with decreased RSV clearance. However, LGSH treatments of the ETOH group normalized oxidant stress, AM immune phenotype, the RSV burden, and acute lung injury. These studies suggest that the oxidant stress caused by fetal ETOH exposure impaired AM clearance of infectious agents, thereby increasing the viral infection and acute lung injury. LGSH treatments reversed the oxidative stress and restored AM immune functions, which decreased the RSV infection and subsequent acute lung injury. Full article

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

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18 pages, 1612 KiB

Open AccessArticle

The Disease Model of Addiction: The Impact of Genetic Variability in the Oxidative Stress and Inflammation Pathways on Alcohol Dependance and Comorbid Psychosymptomatology

by Evangelia Eirini Tsermpini, Katja Goričar, Blanka Kores Plesničar, Anja Plemenitaš Ilješ and Vita Dolžan

Antioxidants 2024, 13(1), 20; https://doi.org/10.3390/antiox13010020 - 21 Dec 2023

Cited by 1 | Viewed by 1597

Abstract

Oxidative stress and neuroinflammation are involved in the pathogenesis of alcohol addiction. However, little is known regarding the effect of genetic, behavioral, psychological, and environmental sources of origin on the inflammation and oxidative stress pathways of patients with alcohol addiction. Our study aimed [...] Read more.

Oxidative stress and neuroinflammation are involved in the pathogenesis of alcohol addiction. However, little is known regarding the effect of genetic, behavioral, psychological, and environmental sources of origin on the inflammation and oxidative stress pathways of patients with alcohol addiction. Our study aimed to evaluate the impact of selected common functional single-nucleotide polymorphisms in inflammation and oxidative stress genes on alcohol addiction, and common comorbid psychosymptomatology. Our study included 89 hospitalized alcohol-addicted patients and 93 healthy individuals, all Slovenian males. Their DNA was isolated from peripheral blood and patients were genotyped for PON1 rs705379, rs705381, rs854560, and rs662, SOD2 rs4880, GPX1 rs1050450, IL1B rs1143623, rs16944, and rs1071676, IL6 rs1800795, IL6R rs2228145, and miR146a rs2910164. Kruskal–Wallis and Mann–Whitney tests were used for the additive and dominant genetic models, respectively. Our findings suggested the involvement of IL6 rs1800795 in alcohol addiction. Moreover, our data indicated that the genetic variability of SOD2 and PON1, as well as IL1B and IL6R, may be related to comorbid psychosymptomatology, revealing a potential indirect means of association of both the oxidative stress and inflammation pathways. Full article

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

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17 pages, 2643 KiB

Open AccessArticle

Fenofibrate Decreases Ethanol-Induced Neuroinflammation and Oxidative Stress and Reduces Alcohol Relapse in Rats by a PPAR-α-Dependent Mechanism

by Cristina Ibáñez, Tirso Acuña, María Elena Quintanilla, Diliana Pérez-Reytor, Paola Morales and Eduardo Karahanian

Antioxidants 2023, 12(9), 1758; https://doi.org/10.3390/antiox12091758 - 13 Sep 2023

Cited by 7 | Viewed by 2344

Abstract

High ethanol consumption triggers neuroinflammation, implicated in sustaining chronic alcohol use. This inflammation boosts glutamate, prompting dopamine release in reward centers, driving prolonged drinking and relapse. Fibrate drugs, activating peroxisome proliferator-activated receptor alpha (PPAR-α), counteract neuroinflammation in other contexts, prompting investigation into their [...] Read more.

High ethanol consumption triggers neuroinflammation, implicated in sustaining chronic alcohol use. This inflammation boosts glutamate, prompting dopamine release in reward centers, driving prolonged drinking and relapse. Fibrate drugs, activating peroxisome proliferator-activated receptor alpha (PPAR-α), counteract neuroinflammation in other contexts, prompting investigation into their impact on ethanol-induced inflammation. Here, we studied, in UChB drinker rats, whether the administration of fenofibrate in the withdrawal stage after chronic ethanol consumption reduces voluntary intake when alcohol is offered again to the animals (relapse-type drinking). Furthermore, we determined if fenofibrate was able to decrease ethanol-induced neuroinflammation and oxidative stress in the brain. Animals treated with fenofibrate decreased alcohol consumption by 80% during post-abstinence relapse. Furthermore, fenofibrate decreased the expression of the proinflammatory cytokines tumor necrosis factor-alpha (TNF-α) and interleukins IL-1β and IL-6, and of an oxidative stress-induced gene (heme oxygenase-1), in the hippocampus, nucleus accumbens, and prefrontal cortex. Animals treated with fenofibrate showed an increase M2-type microglia (with anti-inflammatory proprieties) and a decrease in phagocytic microglia in the hippocampus. A PPAR-α antagonist (GW6471) abrogated the effects of fenofibrate, indicating that they are dependent on PPAR-α activation. These findings highlight the potential of fenofibrate, an FDA-approved dyslipidemia medication, as a supplementary approach to alleviating relapse severity in individuals with alcohol use disorder (AUD) during withdrawal. Full article

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

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17 pages, 2785 KiB

Open AccessArticle

Synergistic Protective Effect of Fermented Schizandrae Fructus Pomace and Hoveniae Semen cum Fructus Extracts Mixture in the Ethanol-Induced Hepatotoxicity

by Kyung-Hwan Jegal, Hye-Rim Park, Beom-Rak Choi, Jae-Kwang Kim and Sae-Kwang Ku

Antioxidants 2023, 12(8), 1602; https://doi.org/10.3390/antiox12081602 - 11 Aug 2023

Cited by 5 | Viewed by 1796

Abstract

Schizandrae Fructus (SF), fruits of Schisandra chinensis (Turcz.) Baill. and Hoveniae Semen cum Fructus (HSCF), the dried peduncle of Hovenia dulcis Thunb., have long been used for alcohol detoxification in the traditional medicine of Korea and China. In the current study, we aimed [...] Read more.

Schizandrae Fructus (SF), fruits of Schisandra chinensis (Turcz.) Baill. and Hoveniae Semen cum Fructus (HSCF), the dried peduncle of Hovenia dulcis Thunb., have long been used for alcohol detoxification in the traditional medicine of Korea and China. In the current study, we aimed to evaluate the potential synergistic hepatoprotective effect of a combination mixture (MSH) comprising fermented SF pomace (fSFP) and HSCF hot water extracts at a 1:1 (w:w) ratio against ethanol-induced liver toxicity. Subacute ethanol-mediated hepatotoxicity was induced by the oral administration of ethanol (5 g/kg) in C57BL/6J mice once daily for 14 consecutive days. One hour after each ethanol administration, MSH (50, 100, and 200 mg/kg) was also orally administered daily. MSH administration significantly reduced the serum activities of alanine aminotransferase, aspartate aminotransferase, alkaline phosphatase, and γ-glutamyl transpeptidase. Histological observation indicated that MSH administration synergistically and significantly decreased the fatty changed region of hepatic parenchyma and the formation of lipid droplet in hepatocytes. Moreover, MSH significantly attenuated the hepatic triglyceride accumulation through reducing lipogenesis genes expression and increasing fatty acid oxidation genes expression. In addition, MSH significantly inhibited protein nitrosylation and lipid peroxidation by lowering cytochrome P450 2E1 enzyme activity and restoring the glutathione level, superoxide dismutase and catalase activity in liver. Furthermore, MSH synergistically decreased the mRNA level of tumor necrosis factor-α in the hepatic tissue. These findings indicate that MSH has potential for preventing alcoholic liver disease through inhibiting hepatic steatosis, oxidative stress, and inflammation. Full article

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

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16 pages, 2387 KiB

Open AccessArticle

Colchicine Protects against Ethanol-Induced Senescence and Senescence-Associated Secretory Phenotype in Endothelial Cells

by Huakang Zhou, Dilaware Khan, Norbert Gerdes, Carsten Hagenbeck, Majeed Rana, Jan Frederick Cornelius and Sajjad Muhammad

Antioxidants 2023, 12(4), 960; https://doi.org/10.3390/antiox12040960 - 19 Apr 2023

Cited by 10 | Viewed by 3039

Abstract

Inflammaging is a potential risk factor for cardiovascular diseases. It results in the development of thrombosis and atherosclerosis. The accumulation of senescent cells in vessels causes vascular inflammaging and contributes to plaque formation and rupture. In addition to being an acquired risk factor [...] Read more.

Inflammaging is a potential risk factor for cardiovascular diseases. It results in the development of thrombosis and atherosclerosis. The accumulation of senescent cells in vessels causes vascular inflammaging and contributes to plaque formation and rupture. In addition to being an acquired risk factor for cardiovascular diseases, ethanol can induce inflammation and senescence, both of which have been implicated in cardiovascular diseases. In the current study, we used colchicine to abate the cellular damaging effects of ethanol on endothelial cells. Colchicine prevented senescence and averted oxidative stress in endothelial cells exposed to ethanol. It lowered the relative protein expression of aging and senescence marker P21 and restored expression of the DNA repair proteins KU70/KU80. Colchicine inhibited the activation of nuclear factor kappa B (NFκ-B) and mitogen activated protein kinases (MAPKs) in ethanol-treated endothelial cells. It reduced ethanol-induced senescence-associated secretory phenotype. In summary, we show that colchicine ameliorated the ethanol-caused molecular events, resulting in attenuated senescence and senescence-associated secretory phenotype in endothelial cells. Full article

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

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Review

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16 pages, 1416 KiB

Open AccessReview

The Impact of Oxidative Stress on the Epigenetics of Fetal Alcohol Spectrum Disorders

by Sergio Terracina, Luigi Tarani, Mauro Ceccanti, Mario Vitali, Silvia Francati, Marco Lucarelli, Sabrina Venditti, Loredana Verdone, Giampiero Ferraguti and Marco Fiore

Antioxidants 2024, 13(4), 410; https://doi.org/10.3390/antiox13040410 - 28 Mar 2024

Viewed by 1785

Abstract

Fetal alcohol spectrum disorders (FASD) represent a continuum of lifelong impairments resulting from prenatal exposure to alcohol, with significant global impact. The “spectrum” of disorders includes a continuum of physical, cognitive, behavioral, and developmental impairments which can have profound and lasting effects on [...] Read more.

Fetal alcohol spectrum disorders (FASD) represent a continuum of lifelong impairments resulting from prenatal exposure to alcohol, with significant global impact. The “spectrum” of disorders includes a continuum of physical, cognitive, behavioral, and developmental impairments which can have profound and lasting effects on individuals throughout their lives, impacting their health, social interactions, psychological well-being, and every aspect of their lives. This narrative paper explores the intricate relationship between oxidative stress and epigenetics in FASD pathogenesis and its therapeutic implications. Oxidative stress, induced by alcohol metabolism, disrupts cellular components, particularly in the vulnerable fetal brain, leading to aberrant development. Furthermore, oxidative stress is implicated in epigenetic changes, including alterations in DNA methylation, histone modifications, and microRNA expression, which influence gene regulation in FASD patients. Moreover, mitochondrial dysfunction and neuroinflammation contribute to epigenetic changes associated with FASD. Understanding these mechanisms holds promise for targeted therapeutic interventions. This includes antioxidant supplementation and lifestyle modifications to mitigate FASD-related impairments. While preclinical studies show promise, further clinical trials are needed to validate these interventions’ efficacy in improving clinical outcomes for individuals affected by FASD. This comprehensive understanding of the role of oxidative stress in epigenetics in FASD underscores the importance of multidisciplinary approaches for diagnosis, management, and prevention strategies. Continued research in this field is crucial for advancing our knowledge and developing effective interventions to address this significant public health concern. Full article

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

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19 pages, 1766 KiB

Open AccessReview

Acetic Acid: An Underestimated Metabolite in Ethanol-Induced Changes in Regulating Cardiovascular Function

by Andrew D. Chapp, Zhiying Shan and Qing-Hui Chen

Antioxidants 2024, 13(2), 139; https://doi.org/10.3390/antiox13020139 - 23 Jan 2024

Viewed by 4436

Abstract

Acetic acid is a bioactive short-chain fatty acid produced in large quantities from ethanol metabolism. In this review, we describe how acetic acid/acetate generates oxidative stress, alters the function of pre-sympathetic neurons, and can potentially influence cardiovascular function in both humans and rodents [...] Read more.

Acetic acid is a bioactive short-chain fatty acid produced in large quantities from ethanol metabolism. In this review, we describe how acetic acid/acetate generates oxidative stress, alters the function of pre-sympathetic neurons, and can potentially influence cardiovascular function in both humans and rodents after ethanol consumption. Our recent findings from in vivo and in vitro studies support the notion that administration of acetic acid/acetate generates oxidative stress and increases sympathetic outflow, leading to alterations in arterial blood pressure. Real-time investigation of how ethanol and acetic acid/acetate modulate neural control of cardiovascular function can be conducted by microinjecting compounds into autonomic control centers of the brain and measuring changes in peripheral sympathetic nerve activity and blood pressure in response to these compounds. Full article

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

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11 pages, 2178 KiB

Open AccessCase Report

Oxidative Stress in a Mother Consuming Alcohol during Pregnancy and in Her Newborn: A Case Report

by Martina Derme, Maria Grazia Piccioni, Roberto Brunelli, Alba Crognale, Marika Denotti, Paola Ciolli, Debora Scomparin, Luigi Tarani, Roberto Paparella, Gianluca Terrin, Maria Di Chiara, Alessandro Mattia, Simona Nicotera, Alberto Salomone, Mauro Ceccanti, Marisa Patrizia Messina, Nunzia La Maida, Giampiero Ferraguti, Carla Petrella and Marco Fiore

Antioxidants 2023, 12(6), 1216; https://doi.org/10.3390/antiox12061216 - 4 Jun 2023

Cited by 7 | Viewed by 2047

Abstract

Fetal alcohol spectrum disorder (FASD) is a set of conditions resulting from prenatal alcohol exposure (PAE). FASD is estimated to affect between 2% and 5% of people in the United States and Western Europe. The exact teratogenic mechanism of alcohol on fetal development [...] Read more.

Fetal alcohol spectrum disorder (FASD) is a set of conditions resulting from prenatal alcohol exposure (PAE). FASD is estimated to affect between 2% and 5% of people in the United States and Western Europe. The exact teratogenic mechanism of alcohol on fetal development is still unclear. Ethanol (EtOH) contributes to the malfunctioning of the neurological system in children exposed in utero by decreasing glutathione peroxidase action, with an increase in the production of reactive oxygen species (ROS), which causes oxidative stress. We report a case of a mother with declared alcohol abuse and cigarette smoking during pregnancy. By analyzing the ethyl glucuronide (EtG, a metabolite of alcohol) and the nicotine/cotinine in the mother’s hair and meconium, we confirmed the alcohol and smoking abuse magnitude. We also found that the mother during pregnancy was a cocaine abuser. As a result, her newborn was diagnosed with fetal alcohol syndrome (FAS). At the time of the delivery, the mother, but not the newborn, had an elevation in oxidative stress. However, the infant, a few days later, displayed marked potentiation in oxidative stress. The clinical complexity of the events involving the infant was presented and discussed, underlining also the importance that for cases of FASD, it is crucial to have more intensive hospital monitoring and controls during the initial days. Full article

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

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