Evaluation of oxidative stress according to the pattern of alcohol consumption and in alcoholic liver disease.
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)....
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Elsevier
2025-04-01
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| Series: | Annals of Hepatology |
| Online Access: | http://www.sciencedirect.com/science/article/pii/S1665268125000596 |
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| author | 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 |
| author_facet | 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 |
| author_sort | Adrián Flores-Sánchez |
| collection | DOAJ |
| description | 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. |
| format | Article |
| id | doaj-art-1b6aa2c477f44048aee611d8ba8e11a3 |
| institution | Kabale University |
| issn | 1665-2681 |
| language | English |
| publishDate | 2025-04-01 |
| publisher | Elsevier |
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| series | Annals of Hepatology |
| spelling | doaj-art-1b6aa2c477f44048aee611d8ba8e11a32025-08-20T03:52:08ZengElsevierAnnals of Hepatology1665-26812025-04-013010183510.1016/j.aohep.2025.101835Evaluation of oxidative stress according to the pattern of alcohol consumption and in alcoholic liver disease.Adrián Flores-Sánchez0Abigail Hernández-Barragán1Daniela Colector-Sesatti2Andrea Garcia-Avalos3Moisés Martínez-Castillo4Marisela Hernández-Santillan5Jaqueline Córdova-Gallardo6José L. Pérez-Hernandez7Fátima Higuera-De la Tijera8Gabriela Gutiérrez-Reyes9Liver, Pancreas, and Motility Laboratory (HIPAM), Experimental Medicine Research Unit, Faculty of Medicine, UNAM, General Hospital of Mexico, Dr. Eduardo Liceaga, MexicoLiver, Pancreas, and Motility Laboratory (HIPAM), Experimental Medicine Research Unit, Faculty of Medicine, UNAM, General Hospital of Mexico, Dr. Eduardo Liceaga, MexicoLiver, Pancreas, and Motility Laboratory (HIPAM), Experimental Medicine Research Unit, Faculty of Medicine, UNAM, General Hospital of Mexico, Dr. Eduardo Liceaga, MexicoLiver, Pancreas, and Motility Laboratory (HIPAM), Experimental Medicine Research Unit, Faculty of Medicine, UNAM, General Hospital of Mexico, Dr. Eduardo Liceaga, MexicoLiver, Pancreas, and Motility Laboratory (HIPAM), Experimental Medicine Research Unit, Faculty of Medicine, UNAM, General Hospital of Mexico, Dr. Eduardo Liceaga, MexicoLiver, Pancreas, and Motility Laboratory (HIPAM), Experimental Medicine Research Unit, Faculty of Medicine, UNAM, General Hospital of Mexico, Dr. Eduardo Liceaga, MexicoDr. Manuel Gea González General Hospital, Mexico City, MexicoGeneral Hospital of México Dr. Eduardo Liceaga, MexicoGeneral Hospital of México Dr. Eduardo Liceaga, MexicoLiver, Pancreas, and Motility Laboratory (HIPAM), Experimental Medicine Research Unit, Faculty of Medicine, UNAM, General Hospital of Mexico, Dr. Eduardo Liceaga, MexicoIntroduction 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.http://www.sciencedirect.com/science/article/pii/S1665268125000596 |
| spellingShingle | 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 Evaluation of oxidative stress according to the pattern of alcohol consumption and in alcoholic liver disease. Annals of Hepatology |
| title | Evaluation of oxidative stress according to the pattern of alcohol consumption and in alcoholic liver disease. |
| title_full | Evaluation of oxidative stress according to the pattern of alcohol consumption and in alcoholic liver disease. |
| title_fullStr | Evaluation of oxidative stress according to the pattern of alcohol consumption and in alcoholic liver disease. |
| title_full_unstemmed | Evaluation of oxidative stress according to the pattern of alcohol consumption and in alcoholic liver disease. |
| title_short | Evaluation of oxidative stress according to the pattern of alcohol consumption and in alcoholic liver disease. |
| title_sort | evaluation of oxidative stress according to the pattern of alcohol consumption and in alcoholic liver disease |
| url | http://www.sciencedirect.com/science/article/pii/S1665268125000596 |
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