title: Alterations in glutathione levels of brain structures caused by acute restraint stress and by nitric oxide synthase inhibition but not by intraspecific agonistic interaction.
abstract: Glutathione is the major non-protein thiol to which many different roles in the central nervous system (CNS) are attributed. To further investigate the glutathione response in the CNS, we tested the effect of three stress models on glutathione levels in the brain. We tested the effect of two models of repeated intraspecific agonistic interaction in mice. No influence was observed over the glutathione levels in the mice cerebral cortex, cerebellum, liver, and blood. Acute restraint stress in rats was found to induce an increase in glutathione levels in the cerebellum after 2 and 4 h of immobilization, an effect not observed in the cerebral cortex, striatum, and hippocampus. To investigate the interference of an inhibitor of nitric oxide synthase (NOS), N(omega)Nitro-L-arginine-methyl-ester (L-NAME, 50 mg/kg) was applied i.p. at the beginning of restraint stress. L-NAME alone did not lead to a change in glutathione levels although, in combination with restraint stress, it induced an increase in such levels. This effect was observed in all four structures studied, i.e. cortex, hippocampus, striatum, and cerebellum. The values returned to basal levels after 6h of immobilization. In conclusion, the pattern of dominance, after repeated intraspecific agonistic interaction, was ineffective in producing alterations in brain glutathione, whereas acute restraint stress led to an increase in glutathione levels within a window of 2-4 h, and the inhibition of NOS increased glutathione levels in all studied rat brain structures, suggesting a specificity interference of acute restraint stress with the glutathione system.
authors.affiliation: Departamento de Ciências Fisiológicas, Centro de Ciências Biológicas, Universidade Federal de Santa Catarina, 88040-900 Florianópolis, SC, Brazil.
authors.forename: Daniel Mathias
authors.initials: DM
authors.lastname: Ghizoni
authors.forename: Kelly Cristine Alves
authors.initials: KC
authors.lastname: Pavanati
authors.forename: André Mendes
authors.initials: AM
authors.lastname: Arent
authors.forename: Claudia
authors.initials: C
authors.lastname: Machado
authors.forename: Moacir Serralvo
authors.initials: MS
authors.lastname: Faria
authors.forename: Cristina Maria Henrique
authors.initials: CM
authors.lastname: Pinto
authors.forename: Odival Cezar
authors.initials: OC
authors.lastname: Gasparotto
authors.forename: Sonia
authors.initials: S
authors.lastname: Gonçalves
authors.forename: Alcir Luiz
authors.initials: AL
authors.lastname: Dafre
mesh_terms: D000378:Agonistic Behavior / Q000187:drug effects / Q000502:physiology; D000704:Analysis of Variance; D000818:Animals; D001522:Behavior, Animal; D001921:Brain / Q000033:anatomy & histology / Q000187:drug effects / Q000378:metabolism*; D005978:Glutathione / Q000378:metabolism*; D008297:Male; D051379:Mice; D019331:NG-Nitroarginine Methyl Ester / Q000494:pharmacology; D009433:Neural Inhibition / Q000187:drug effects / Q000502:physiology*; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors / Q000502:physiology*; D051381:Rats; D017208:Rats, Wistar; D012149:Restraint, Physical / Q000379:methods; D013312:Stress, Physiological / Q000378:metabolism*
chemical_list: D019001:Nitric Oxide Synthase; D005978:Glutathione; D019331:NG-Nitroarginine Methyl Ester