Producción CyT
Congreso
Autoría
Fecha
2017
Editorial y Lugar de Edición
Estudio Sigma S.R.L.
ISSN
1669-9106
Resumen
Información suministrada por el agente en
SIGEVA
Glutamate is an excitatory neurotransmitter in central nervous system. Glutamate excitotoxicity is thought to play an important role in neuronal damage. N-acetyl cysteine (NAC) could be useful as a donor of sulfhydryl groups, increasing glutathione levels. The aims were to evaluate changes in redox status in brain of rats subjected to a model of glutamate excitotoxicity and to identify modifications when an antioxidant therapy was given. The experimental model consisted of four groups: Glutamat...
Glutamate is an excitatory neurotransmitter in central nervous system. Glutamate excitotoxicity is thought to play an important role in neuronal damage. N-acetyl cysteine (NAC) could be useful as a donor of sulfhydryl groups, increasing glutathione levels. The aims were to evaluate changes in redox status in brain of rats subjected to a model of glutamate excitotoxicity and to identify modifications when an antioxidant therapy was given. The experimental model consisted of four groups: Glutamate Group was injected with 1g/kg weight of monosodium glutamate, Control Group was injected with saline solution, Treated Glutamate Group was supplemented with 150 mg/kg weight of NAC and with 1 g/kg weight of monosodium glutamate and Treated Control Group was supplemented with 150 mg/kg weight of NAC. The supplementation was given every day while the glutamate was injected at days 1, 5 and 9. CICUAL approved every experimental procedure. The following markers were evaluated in brain homogenates: the activities of superoxide dismutase (SOD), glutathione reductase (GR), NADPH oxidase, protein oxidative damage, and glutathione levels. Glutamate increased SOD (28%,p<0.05), GR (15%,p<0.01), NADPH oxidase (31%,p<0.01), protein oxidation (24%,p<0.05), and decreased glutathione (24%, p<0.05) compared to control group. NAC decreased SOD (19%,p<0.05), GR (25%,p<0.05), NADPH oxidase (48%,p<0.01), and increased glutathione (28%,p<0.05) compared to glutamate group. NAC also increased glutathione (30%,p<0.05) respect control group. No changes were found in protein damage.Decrease in non-enzymatic antioxidants as well as the compensatory up-regulation of antioxidant enzymes activities could be consequence of an increase in oxidative processes in glutamate excitotoxicity model. NAC could be useful to maintain the redox status as it increases glutathione and produces a decrease in the enzymes related to reactive oxygen species production.
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Palabras Clave
REDOX STATUSGLUTAMATEANTIOXIDANTBRAIN