Supplementation with omega-3 has been identified as an adjunctive alternative for the treatment of psychiatric disorders, in order to minimize symptoms. Considering the lack of understanding concerning the pathophysiology of schizophrenia, the present study hypothesized that omega 3 prevents the onset of symptoms similar to schizophrenia in young Wistar rats submitted to ketamine treatment. Moreover, the role of oxidative stress in this model was assessed. Omega-3 (0.8g/kg) or vehicle was given by orogastric gavage once daily. Both treatments were performed during 21days, starting at the 30th day of life in young rats. After 14days of treatment with omega-3 or vehicle, a concomitant treatment with saline or ketamine (25mg/kg ip daily) was started and maintained until the last day of the experiment. We evaluated the pre-pulse inhibition of the startle reflex, activity of antioxidant systems and damage to proteins and lipids. Our results demonstrate that supplementation of omega-3 prevented: decreased inhibition of startle reflex, damage to lipids in the hippocampus and striatum and damage to proteins in the prefrontal cortex. Furthermore, these changes are associated with decreased GPx in brain tissues evaluated. Together, our results suggest the prophylactic role of omega-3 against the outcome of symptoms associated with schizophrenia.
Keywords: ANOVA; BDNF; Brain-derived neurotrophic factor; CAT; DHA; DNPH; EDTA; EPA; GPx; GSH; NADPH; PUFAs; ROS; SOD; TBARS; analysis of variance; antioxidants; catalase; dihydronicotinamide-adenine dinucleotide phosphate; dinitrophenylhydrazine; docosahexaenoic acid; eicosapentaenoic acid; ethylenediaminetetraacetic acid; glutathione; glutathione peroxidase; ketamine; omega 3; polyunsaturated fatty acids; prepulse inhibition; reactive oxygen species; schizophrenia; superoxide dismutase; thiobarbituric acid reactive species.
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