Antioxidant status of the brain in a glutamate excitotoxicity model and the effect of n-acetyl-cysteine.

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

Congreso; 19th International Conference on Oxidative Stress Reduction, Redox Homeostasis and Antioxidants Paris Redox; 2017

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. 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. 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. 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.