Protective Effects of Ascorbic Acid on Behavior and Oxidative Status of Restraint-Stressed Mice

• Published in: Journal of molecular neuroscience 2013-01, Vol.49 (1), p.68-79
• Main Authors: Moretti, Morgana, Budni, Josiane, dos Santos, Danubia Bonfanti, Antunes, Alessandra, Daufenbach, Juliana Felipe, Manosso, Luana Meller, Farina, Marcelo, Rodrigues, Ana Lúcia S.
• Format: Article
• Language: English
• Subjects: Acids; Animals; Antidepressants; Antioxidants; Antioxidants - pharmacology; Antioxidants - therapeutic use; Ascorbic acid; Ascorbic Acid - pharmacology; Ascorbic Acid - therapeutic use; Bax protein; Bcl-2 protein; bcl-2-Associated X Protein - genetics; bcl-2-Associated X Protein - metabolism; Behavior; Biomedical and Life Sciences; Biomedicine; Cell Biology; Cell death; Cerebral Cortex - enzymology; Cerebral Cortex - metabolism; Cortex; Depression; Depressive Disorder - drug therapy; Depressive Disorder - etiology; Emotional disorders; Enzymes; Female; Fluoxetine; Glutathione peroxidase; Glutathione Peroxidase - genetics; Glutathione Peroxidase - metabolism; glutathione reductase; Glutathione Reductase - genetics; Glutathione Reductase - metabolism; Glycogen synthase kinase 3; Glycogen Synthase Kinase 3 - genetics; Glycogen Synthase Kinase 3 - metabolism; Glycogen Synthase Kinase 3 beta; Hippocampus; Hippocampus - enzymology; Hippocampus - metabolism; Kinases; Laboratory animals; Lipid Metabolism - drug effects; Lipid peroxidation; Lipids; Mental depression; Mice; Mood disorders; Motor Activity - drug effects; Nervous system; Neurochemistry; Neurology; Neurosciences; Oxidation-Reduction - drug effects; Oxidative stress; Phosphorylation; Proteomics; Proto-Oncogene Proteins c-bcl-2 - genetics; Proto-Oncogene Proteins c-bcl-2 - metabolism; Stress, Psychological - complications; Superoxide dismutase; Superoxide Dismutase - genetics; Superoxide Dismutase - metabolism; Swimming; Transcription, Genetic - drug effects; Vitamins; Vitamins - pharmacology; Vitamins - therapeutic use
• ISSN: 0895-8696; 1559-1166
• DOI: 10.1007/s12031-012-9892-4

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.