Protective effects of ascorbic acid on behavior and oxidative status of restraint-stressed mice.
Studies have demonstrated an association between stressful conditions and the onset of clinical depression. Considering the antidepressant-like properties of ascorbic acid in both experimental and clinical approaches, we evaluated the beneficial effect of this vitamin on restraint stress-induced behavioral and neurochemical alterations. Acute restraint stress caused a depressive-like behavior in the forced swimming test, accompanied by increased lipid peroxidation (cerebral cortex and hippocampus); increased superoxide dismutase (cerebral cortex and hippocampus), glutathione reductase (cerebral cortex), and glutathione peroxidase (cerebral cortex and hippocampus) activities; and elevated expression of Bcl-2 (hippocampus). Oral administration of ascorbic acid (1 mg/kg) or fluoxetine (10 mg/kg) 1 h before restraint stress prevented the stress-induced increase on immobility time in the forced swimming test. Moreover, this vitamin reduced lipid peroxidation to control levels and restored the activity of superoxide dismutase, glutathione reductase, and glutathione peroxidase. Ascorbic acid had no effect on the increased level of Bcl-2 induced by stress. Glutathione levels, glycogen synthase kinase-3β phosphorylation, and Bax expression were not altered by stress or ascorbic acid administration. Besides reinforcing the antioxidant potential of ascorbic acid, our results support the notion that oxidative stress plays a role in the pathogenesis and treatment of stress-induced depression.
Departamento de Bioquímica, Centro de Ciências Biológicas, Universidade Federal de Santa Catarina, Florianópolis, 88040-900 SC, Brazil.
Morgana
M
Moretti
Josiane
J
Budni
Danubia Bonfanti
DB
Dos Santos
Alessandra
A
Antunes
Juliana Felipe
JF
Daufenbach
Luana Meller
LM
Manosso
Marcelo
M
Farina
Ana Lúcia S
AL
Rodrigues
D000818:Animals; D000975:Antioxidants / Q000494:pharmacology / Q000627:therapeutic use*; D001205:Ascorbic Acid / Q000494:pharmacology / Q000627:therapeutic use*; D002540:Cerebral Cortex / Q000201:enzymology / Q000378:metabolism; D003866:Depressive Disorder / Q000188:drug therapy* / Q000209:etiology; D005260:Female; D005979:Glutathione Peroxidase / Q000235:genetics / Q000378:metabolism; D005980:Glutathione Reductase / Q000235:genetics / Q000378:metabolism; D038362:Glycogen Synthase Kinase 3 / Q000235:genetics / Q000378:metabolism; D000071679:Glycogen Synthase Kinase 3 beta; D006624:Hippocampus / Q000201:enzymology / Q000378:metabolism; D050356:Lipid Metabolism / Q000187:drug effects; D051379:Mice; D009043:Motor Activity / Q000187:drug effects; D010084:Oxidation-Reduction / Q000187:drug effects; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000235:genetics / Q000378:metabolism; D013315:Stress, Psychological / Q000150:complications*; D013482:Superoxide Dismutase / Q000235:genetics / Q000378:metabolism; D013550:Swimming; D014158:Transcription, Genetic / Q000187:drug effects; D014815:Vitamins / Q000494:pharmacology / Q000627:therapeutic use*; D051028:bcl-2-Associated X Protein / Q000235:genetics / Q000378:metabolism
D000975:Antioxidants; C494827:Bax protein, mouse; D019253:Proto-Oncogene Proteins c-bcl-2; D014815:Vitamins; D051028:bcl-2-Associated X Protein; C052617:Bcl2 protein, mouse; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase; D005980:Glutathione Reductase; D000071679:Glycogen Synthase Kinase 3 beta; C000605507:Gsk3b protein, mouse; D038362:Glycogen Synthase Kinase 3; D001205:Ascorbic Acid