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Acute restraint stress reduces hippocampal oxidative damage and behavior in rats: Effect of S-allyl cysteine

Colín-González, Ana Laura, Becerríl, Hugo, Flores-Reyes, Bianca Rubí, Torres, Ismael, Pinzón, Enrique, Angel, Daniel Santamaría-Del, Túnez, Isaac, Serratos, Iris, Pedraza-Chaverrí, José, Santamaría, Abel, Maldonado, Perla D.
Life sciences 2015 v.135 pp. 165-172
antioxidants, anxiety, cysteine, enzyme activity, glutathione, glutathione peroxidase, glutathione transferase, hippocampus, lipid peroxidation, oxidative stress, rats, restraint of animals, swimming
This simple study was designed to investigate whether acute restraint stress can generate changes in behavioral tests and hippocampal endpoints of oxidative stress in rats, and if the antioxidant S-allyl cysteine (SAC) can prevent these alterations.We evaluated motor activity, forced swimming and anxiety behavior, as well as the hippocampal levels of lipid peroxidation and the activities of glutathione-related enzymes in animals submitted to mild immobilization. The effect of SAC (100mg/kg, i.p.), given to rats every day 30min before starting the immobilization session, was also investigated. Immobilization (restraint) stress was induced for a period of 6h per day for five consecutive days.Our results indicate that, under the tested conditions, acute restraint stimulates compensatory behavioral tasks (motor activity, anxiety and forced swimming) to counteract the stressing conditions prevailing, and selectively increased the levels of lipid peroxidation and the enzyme activities of glutathione-S-transferase (GST) and glutathione peroxidase (GPx) in the hippocampus also as adaptive responses. SAC exhibited preventive effects in the stressed group as it improved behavior, reduced lipid peroxidation and prevented the increase of GST and GPx activities, suggesting that this antioxidant blunted primary pro-oxidative stimuli induced by restraint stress.Findings of this work also confirm that the use of antioxidants such as SAC can provide effective protection against the acute oxidative damage associated with anxiety produced by stressing conditions.