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

A special issue of Antioxidants (ISSN 2076-3921).

Deadline for manuscript submissions: 20 February 2025 | Viewed by 819

Special Issue Editor

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

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Keywords

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

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Published Papers (1 paper)

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Research

18 pages, 3245 KiB  
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
Viewed by 521
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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