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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 beh...
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| Published in: | Journal of molecular neuroscience 2013-01, Vol.49 (1), p.68-79 |
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| container_title | Journal of molecular neuroscience |
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| creator | Moretti, Morgana Budni, Josiane dos Santos, Danubia Bonfanti Antunes, Alessandra Daufenbach, Juliana Felipe Manosso, Luana Meller Farina, Marcelo Rodrigues, Ana Lúcia S. |
| description | 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. |
| doi_str_mv | 10.1007/s12031-012-9892-4 |
| format | article |
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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.</description><identifier>ISSN: 0895-8696</identifier><identifier>EISSN: 1559-1166</identifier><identifier>DOI: 10.1007/s12031-012-9892-4</identifier><identifier>PMID: 23054587</identifier><language>eng</language><publisher>New York: Humana Press Inc</publisher><subject>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</subject><ispartof>Journal of molecular neuroscience, 2013-01, Vol.49 (1), p.68-79</ispartof><rights>Springer Science+Business Media New York 2012</rights><rights>Springer Science+Business Media New York 2013</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c471t-39f9bb4c1e264666cc1bdd6ff376351edb209a22b87a3c249153526375c9a66c3</citedby><cites>FETCH-LOGICAL-c471t-39f9bb4c1e264666cc1bdd6ff376351edb209a22b87a3c249153526375c9a66c3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>315,786,790,27957,27958</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23054587$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Moretti, Morgana</creatorcontrib><creatorcontrib>Budni, Josiane</creatorcontrib><creatorcontrib>dos Santos, Danubia Bonfanti</creatorcontrib><creatorcontrib>Antunes, Alessandra</creatorcontrib><creatorcontrib>Daufenbach, Juliana Felipe</creatorcontrib><creatorcontrib>Manosso, Luana Meller</creatorcontrib><creatorcontrib>Farina, Marcelo</creatorcontrib><creatorcontrib>Rodrigues, Ana Lúcia S.</creatorcontrib><title>Protective Effects of Ascorbic Acid on Behavior and Oxidative Status of Restraint-Stressed Mice</title><title>Journal of molecular neuroscience</title><addtitle>J Mol Neurosci</addtitle><addtitle>J Mol Neurosci</addtitle><description>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.</description><subject>Acids</subject><subject>Animals</subject><subject>Antidepressants</subject><subject>Antioxidants</subject><subject>Antioxidants - pharmacology</subject><subject>Antioxidants - therapeutic use</subject><subject>Ascorbic acid</subject><subject>Ascorbic Acid - pharmacology</subject><subject>Ascorbic Acid - therapeutic use</subject><subject>Bax protein</subject><subject>Bcl-2 protein</subject><subject>bcl-2-Associated X Protein - genetics</subject><subject>bcl-2-Associated X Protein - metabolism</subject><subject>Behavior</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Cell Biology</subject><subject>Cell death</subject><subject>Cerebral Cortex - enzymology</subject><subject>Cerebral Cortex - metabolism</subject><subject>Cortex</subject><subject>Depression</subject><subject>Depressive Disorder - drug therapy</subject><subject>Depressive Disorder - etiology</subject><subject>Emotional disorders</subject><subject>Enzymes</subject><subject>Female</subject><subject>Fluoxetine</subject><subject>Glutathione peroxidase</subject><subject>Glutathione Peroxidase - genetics</subject><subject>Glutathione Peroxidase - metabolism</subject><subject>glutathione reductase</subject><subject>Glutathione Reductase - genetics</subject><subject>Glutathione Reductase - metabolism</subject><subject>Glycogen synthase kinase 3</subject><subject>Glycogen Synthase Kinase 3 - genetics</subject><subject>Glycogen Synthase Kinase 3 - metabolism</subject><subject>Glycogen Synthase Kinase 3 beta</subject><subject>Hippocampus</subject><subject>Hippocampus - enzymology</subject><subject>Hippocampus - metabolism</subject><subject>Kinases</subject><subject>Laboratory animals</subject><subject>Lipid Metabolism - drug effects</subject><subject>Lipid peroxidation</subject><subject>Lipids</subject><subject>Mental depression</subject><subject>Mice</subject><subject>Mood disorders</subject><subject>Motor Activity - drug effects</subject><subject>Nervous system</subject><subject>Neurochemistry</subject><subject>Neurology</subject><subject>Neurosciences</subject><subject>Oxidation-Reduction - drug effects</subject><subject>Oxidative stress</subject><subject>Phosphorylation</subject><subject>Proteomics</subject><subject>Proto-Oncogene Proteins c-bcl-2 - genetics</subject><subject>Proto-Oncogene Proteins c-bcl-2 - metabolism</subject><subject>Stress, Psychological - complications</subject><subject>Superoxide dismutase</subject><subject>Superoxide Dismutase - genetics</subject><subject>Superoxide Dismutase - metabolism</subject><subject>Swimming</subject><subject>Transcription, Genetic - drug effects</subject><subject>Vitamins</subject><subject>Vitamins - pharmacology</subject><subject>Vitamins - therapeutic use</subject><issn>0895-8696</issn><issn>1559-1166</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><recordid>eNp1kM1qGzEURkVJaZy0D9BNEWSTjRJdaaSRlq5xfiDBIW7XQqPRJAr2yJVmTPP2Uey0lEBXuqDzffdyEPoK9Aworc8zMMqBUGBEK81I9QFNQAhNAKQ8QBOqtCBKanmIjnJ-opRBBeoTOmScikqoeoLMXYqDd0PYejzvujJlHDs8zS6mJjg8daHFscff_aPdhpiw7Vu8-B1au4ssBzuMu8S9z0OyoR_Ickg-Z9_i2-D8Z_Sxs6vsv7y9x-jnxfzH7IrcLC6vZ9Mb4qoaBsJ1p5umcuCZrKSUzkHTtrLreC25AN82jGrLWKNqyx2rNAgumOS1cNoWnB-j033vJsVfY7nFrEN2frWyvY9jNsA0SCpqJgp68g59imPqy3WFkrJWCqQqFOwpl2LOyXdmk8LapmcD1LzaN3v7ptg3r_ZNVTLf3prHZu3bv4k_ugvA9kAuX_2DT_-s_m_rCyfbjis</recordid><startdate>20130101</startdate><enddate>20130101</enddate><creator>Moretti, Morgana</creator><creator>Budni, Josiane</creator><creator>dos Santos, Danubia Bonfanti</creator><creator>Antunes, Alessandra</creator><creator>Daufenbach, Juliana Felipe</creator><creator>Manosso, Luana Meller</creator><creator>Farina, Marcelo</creator><creator>Rodrigues, Ana Lúcia S.</creator><general>Humana Press Inc</general><general>Springer Nature B.V</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7QL</scope><scope>7QR</scope><scope>7T7</scope><scope>7TK</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>88G</scope><scope>8AO</scope><scope>8FD</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>C1K</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M2M</scope><scope>M7N</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PSYQQ</scope><scope>Q9U</scope></search><sort><creationdate>20130101</creationdate><title>Protective Effects of Ascorbic Acid on Behavior and Oxidative Status of Restraint-Stressed Mice</title><author>Moretti, Morgana ; Budni, Josiane ; dos Santos, Danubia Bonfanti ; Antunes, Alessandra ; Daufenbach, Juliana Felipe ; Manosso, Luana Meller ; Farina, Marcelo ; Rodrigues, Ana Lúcia S.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c471t-39f9bb4c1e264666cc1bdd6ff376351edb209a22b87a3c249153526375c9a66c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>Acids</topic><topic>Animals</topic><topic>Antidepressants</topic><topic>Antioxidants</topic><topic>Antioxidants - pharmacology</topic><topic>Antioxidants - therapeutic use</topic><topic>Ascorbic acid</topic><topic>Ascorbic Acid - pharmacology</topic><topic>Ascorbic Acid - therapeutic use</topic><topic>Bax protein</topic><topic>Bcl-2 protein</topic><topic>bcl-2-Associated X Protein - genetics</topic><topic>bcl-2-Associated X Protein - metabolism</topic><topic>Behavior</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Cell Biology</topic><topic>Cell death</topic><topic>Cerebral Cortex - enzymology</topic><topic>Cerebral Cortex - metabolism</topic><topic>Cortex</topic><topic>Depression</topic><topic>Depressive Disorder - drug therapy</topic><topic>Depressive Disorder - etiology</topic><topic>Emotional disorders</topic><topic>Enzymes</topic><topic>Female</topic><topic>Fluoxetine</topic><topic>Glutathione peroxidase</topic><topic>Glutathione Peroxidase - genetics</topic><topic>Glutathione Peroxidase - metabolism</topic><topic>glutathione reductase</topic><topic>Glutathione Reductase - genetics</topic><topic>Glutathione Reductase - metabolism</topic><topic>Glycogen synthase kinase 3</topic><topic>Glycogen Synthase Kinase 3 - genetics</topic><topic>Glycogen Synthase Kinase 3 - metabolism</topic><topic>Glycogen Synthase Kinase 3 beta</topic><topic>Hippocampus</topic><topic>Hippocampus - enzymology</topic><topic>Hippocampus - metabolism</topic><topic>Kinases</topic><topic>Laboratory animals</topic><topic>Lipid Metabolism - drug effects</topic><topic>Lipid peroxidation</topic><topic>Lipids</topic><topic>Mental depression</topic><topic>Mice</topic><topic>Mood disorders</topic><topic>Motor Activity - drug effects</topic><topic>Nervous system</topic><topic>Neurochemistry</topic><topic>Neurology</topic><topic>Neurosciences</topic><topic>Oxidation-Reduction - drug effects</topic><topic>Oxidative stress</topic><topic>Phosphorylation</topic><topic>Proteomics</topic><topic>Proto-Oncogene Proteins c-bcl-2 - genetics</topic><topic>Proto-Oncogene Proteins c-bcl-2 - metabolism</topic><topic>Stress, Psychological - complications</topic><topic>Superoxide dismutase</topic><topic>Superoxide Dismutase - genetics</topic><topic>Superoxide Dismutase - metabolism</topic><topic>Swimming</topic><topic>Transcription, Genetic - drug effects</topic><topic>Vitamins</topic><topic>Vitamins - pharmacology</topic><topic>Vitamins - therapeutic use</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Moretti, Morgana</creatorcontrib><creatorcontrib>Budni, Josiane</creatorcontrib><creatorcontrib>dos Santos, Danubia Bonfanti</creatorcontrib><creatorcontrib>Antunes, Alessandra</creatorcontrib><creatorcontrib>Daufenbach, Juliana Felipe</creatorcontrib><creatorcontrib>Manosso, Luana Meller</creatorcontrib><creatorcontrib>Farina, Marcelo</creatorcontrib><creatorcontrib>Rodrigues, Ana Lúcia S.</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Chemoreception Abstracts</collection><collection>Industrial and Applied Microbiology Abstracts (Microbiology A)</collection><collection>Neurosciences Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>ProQuest Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Psychology Database (Alumni)</collection><collection>ProQuest Pharma Collection</collection><collection>Technology Research Database</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>AUTh Library subscriptions: ProQuest Central</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>PML(ProQuest Medical Library)</collection><collection>Psychology Journals (ProQuest)</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest One Psychology</collection><collection>ProQuest Central Basic</collection><jtitle>Journal of molecular neuroscience</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Moretti, Morgana</au><au>Budni, Josiane</au><au>dos Santos, Danubia Bonfanti</au><au>Antunes, Alessandra</au><au>Daufenbach, Juliana Felipe</au><au>Manosso, Luana Meller</au><au>Farina, Marcelo</au><au>Rodrigues, Ana Lúcia S.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Protective Effects of Ascorbic Acid on Behavior and Oxidative Status of Restraint-Stressed Mice</atitle><jtitle>Journal of molecular neuroscience</jtitle><stitle>J Mol Neurosci</stitle><addtitle>J Mol Neurosci</addtitle><date>2013-01-01</date><risdate>2013</risdate><volume>49</volume><issue>1</issue><spage>68</spage><epage>79</epage><pages>68-79</pages><issn>0895-8696</issn><eissn>1559-1166</eissn><notes>ObjectType-Article-2</notes><notes>SourceType-Scholarly Journals-1</notes><notes>ObjectType-Feature-1</notes><notes>content type line 23</notes><abstract>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.</abstract><cop>New York</cop><pub>Humana Press Inc</pub><pmid>23054587</pmid><doi>10.1007/s12031-012-9892-4</doi><tpages>12</tpages></addata></record> |
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| 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 |
| title | Protective Effects of Ascorbic Acid on Behavior and Oxidative Status of Restraint-Stressed Mice |
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