Oral administration of resveratrol reduces oxidative stress generated in the hippocampus of Wistar rats in response to consumption of ethanol

• Published in: Frontiers in behavioral neuroscience Vol. 17; p. 1304006
• Main Authors: Navarro-Cruz, Addí Rhode, Juárez-Serrano, Daniel, Cesar-Arteaga, Ivan, Kammar-García, Ashuin, Guevara-Díaz, Jorge Alberto, Vera-López, Obdulia, Lazcano-Hernández, Martin, Pérez-Xochipa, Ivonne, Segura-Badilla, Orietta
• Format: Journal Article
• Language: English
• Published: Switzerland Frontiers Research Foundation 11.01.2024; Frontiers Media S.A
• Subjects: Alcohol; Antioxidants; Apoptosis; Behavioral Neuroscience; Catalase; Enzymatic activity; Enzymes; Ethanol; Free radicals; Glutathione; Hippocampus; Ketamine; Laboratory animals; Lipid peroxidation; Nitric oxide; Nitrites; Oral administration; Oxidative stress; Polyphenols; Proteins; reactive oxygen species; Reagents; Resveratrol; United States > US; hippocampus; ethanol; resveratrol; oxidative stress; reactive oxygen species
• ISSN: 1662-5153; 1662-5153
• DOI: 10.3389/fnbeh.2023.1304006

Chronic ethanol intake has been found to favor hippocampal deterioration and alter neuronal morphological maturation; resveratrol has been suggested as an antioxidant that may counteract these effects. The objective of this study was to analyze the effect of resveratrol on oxidative stress markers, endogenous antioxidant system in the hippocampus, and the behavior of male Wistar rats administered different concentrations of ethanol. The animals, at 3 months old, were randomly distributed into 11 study groups (  = 6/group), orally administered (5 days on, 2 days off) with water (control), ethanol (10, 20, 30, 40 or 50%), or ethanol (10, 20, 30, 40 or 50%) plus resveratrol (10 mg/Kg/day) for 2 months. Subsequently, the production of nitrites, malondialdehyde, and 4-hydroxy-alkenal (HNE) and the enzymatic activity of catalase and superoxide dismutase (SOD) were quantified. The levels of nitric oxide and lipid peroxidation products were significantly increased in each ethanol concentration and were statistically different compared to the control group; however, resveratrol significantly reduced oxidative stress caused by high ethanol concentration. The SOD and CAT did not present significant changes with respect to the controls in any of the study groups. In the different concentrations of ethanol used, GR increases significantly in the groups administered with resveratrol but not GPx. Resveratrol was shown to maintain the results similar to the control at most ethanol concentrations. Our results suggest that resveratrol prevents oxidative stress induced by ethanol in the hippocampus by decreasing cellular lipid peroxidation, but does not prevent the activation of catalase or SOD enzymes; however, allows glutathione to be kept active and in adequate concentrations in its reduced form and avoids alterations in the locomotor system.