ANTIOXIDANT STATUS OF THE BRAIN IN A GLUTAMATE EXCITOTOXICITY MODEL AND THE EFFECT OF N-ACETYL-CYSTEINE.

HVOZDA ARANA AILEN, ; REIDES, CLAUDIA; FERREIRA, SANDRA; LLESUY, SUSANA,; PEVERINI AGUSTINA ; WEISCHLER NATHALIE ; JANEZIC NATASHA ; LASAGNI VITAR, ROMINA M.

Paris

Congreso; Paris Redox 2017 - 19th International Conference on Antioxidants; 2017

International Society of Antioxidants

Introduction: The aims were to evaluate changes in antioxidant status in brain of rats subjected to a model of glutamate excitotoxicity and to identify modifications when an antioxidant therapy was given. Material & Methods: Four groups were performed: GG was injected with 1g/kg of monosodium glutamate, CG was injected with saline solution, TG was supplemented with 150 mg/kg of N-acetyl cysteine and with 1 g/kg of monosodium glutamate and TC was supplemented with 150 mg/kg of N-acetyl cysteine. Levels of antioxidants, the activities of antioxidant enzymes, and protein damage were measured. Results: Glutamate increased superoxide dismutase (28% p< 0.05), catalase (95% p< 0.05), NADPH oxidase (29% p< 0.001), protein oxidation (22% p< 0.05), and decreased glutathione (30% p< 0.05)N-acetyl cysteine decreased superoxide dismutase (19% p< 0.05), NADPH oxidase (45% p< 0.001), glutathione reductase (25% p< 0.05) activities and increased glutathione (30% p< 0.05). No changes were found in protein damage.Conclusion: Decrease in non-enzymatic antioxidants and compensatory up-regulation of antioxidant enzymes activities may be consequence of an increase in oxidative process in glutamate excitotoxicity. N-acetyl cysteine could be useful as a donor of sulfhydryl groups, increasing glutathione, and produced a decay in enzymes related with reactive oxygen species production.