Evaluation of oxidative stress according to the pattern of alcohol consumption and in alcoholic liver disease.

IF 3.7 3区医学 Q2 GASTROENTEROLOGY & HEPATOLOGY

Annals of hepatology Pub Date : 2025-04-01 DOI:10.1016/j.aohep.2025.101835

Adrián Flores-Sánchez , Abigail Hernández-Barragán , Daniela Colector-Sesatti , Andrea Garcia-Avalos , Moisés Martínez-Castillo , Marisela Hernández-Santillan , Jaqueline Córdova-Gallardo , José L. Pérez-Hernandez , Fátima Higuera-De la Tijera , Gabriela Gutiérrez-Reyes

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Abstract

Introduction and Objectives

Alcohol and its metabolites induce damage in the liver, such as: activation of the immune response and oxidative stress. Objective: To evaluate the redox state through markers of oxidative stress in patterns of alcohol consumption and alcohol-related liver disease (ALD).

Materials and Patients

A cross-sectional and multicenter study was conducted, with the inclusion of individuals displaying various patterns of alcohol consumption. Participants were categorized based on responses to questionnaires (AUDIT and DSM-IV), as well as an individualized survey, along with clinical and biochemical data. Six distinct groups were established: Risk (RI), Abuse (Ab), Alcoholism (OH), as well as ALD: alcohol liver cirrhosis (CiOH) and alcoholic hepatitis (HA), in addition to a control group (CT). Stress markers, including reduced glutathione (GSH) and oxidized glutathione (GSSG), were assessed in peripheral blood and we calculated GSH/GSSG ratio, lipid peroxidation via malondialdehyde formation, and protein oxidized by carbonylated protein were quantified. Statistical analysis was performed utilizing the Mann-Whitney U test, with statistical significance set at p<0.05.

Results

The subjects were classified into RI (22), Ab (4), OH (28), CiOH (76), HA (16), and CT (100). The GSH was found to decrease significantly in the EHA groups vs CT. In contrast, GSSG increased in the RI, Ab, OH, and CiOH groups compared to CT, indicating that alcohol consumption favors an oxidizing state, confirmed by the negative GSH/GSSG ratio. Additionally, the GSH/GSSG ratio in the OH group showed a greater imbalance than in patients with EHA. On the other hand, protein oxidation increased in EHA, with high levels of carbonylated proteins observed in OH, CiOH, and HA compared to CT, Ab, and RI. Furthermore, lipoperoxidation measured by Malondialdehyde showed increased levels of OH and CiOH compared to the other study groups.

Conclusions

Excessive alcohol consumption, with or without liver damage, promotes the oxidation of proteins and lipids. Additionally, alcohol favors the oxidized form of the main endogenous antioxidant, GSH. Therefore, it is necessary to control the redox balance through antioxidant treatment.

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根据饮酒模式和酒精性肝病评估氧化应激。

酒精及其代谢物可引起肝脏损伤，如：免疫反应激活和氧化应激。目的：通过酒精消耗和酒精相关性肝病（ALD）模式中的氧化应激标志物来评估氧化还原状态。材料和患者进行了一项横断面和多中心研究，纳入了表现出不同饮酒模式的个体。参与者根据问卷调查（AUDIT和DSM-IV）、个性化调查以及临床和生化数据进行分类。除对照组（CT）外，还建立了六个不同的组：危险组（RI）、滥用组（Ab）、酒精中毒组（OH）以及ALD：酒精性肝硬化（CiOH）和酒精性肝炎（HA）。测定外周血中的应激标志物，包括还原性谷胱甘肽（GSH）和氧化性谷胱甘肽（GSSG），并计算GSH/GSSG比值、丙二醛形成的脂质过氧化和羰基化蛋白氧化的蛋白质。采用Mann-Whitney U检验进行统计学分析，统计学显著性设置为p<；0.05。结果研究对象分为RI（22）、Ab(4)、OH（28）、CiOH（76）、HA（16）、CT（100）。与CT相比，EHA组的GSH明显降低。相比之下，与CT相比，RI、Ab、OH和CiOH组的GSSG增加，表明酒精消耗有利于氧化状态，GSH/GSSG的负比值证实了这一点。此外，与EHA患者相比，OH组的GSH/GSSG比例表现出更大的失衡。另一方面，EHA中的蛋白质氧化增加，与CT、Ab和RI相比，在OH、CiOH和HA中观察到高水平的羰基化蛋白质。此外，与其他研究组相比，丙二醛测量的脂质过氧化显示OH和CiOH水平增加。结论无论有无肝损伤，过量饮酒均可促进蛋白质和脂质氧化。此外，酒精有利于氧化形式的主要内源性抗氧化剂，谷胱甘肽。因此，有必要通过抗氧化处理来控制氧化还原平衡。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Annals of hepatology 医学-胃肠肝病学

CiteScore

7.90

自引率

2.60%

发文量

183

审稿时长

4-8 weeks

期刊介绍： Annals of Hepatology publishes original research on the biology and diseases of the liver in both humans and experimental models. Contributions may be submitted as regular articles. The journal also publishes concise reviews of both basic and clinical topics.