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Clomipramine Treatment and Repeated Restraint Stress Alter Parameters of Oxidative Stress in Brain Regions of Male Rats
This study aimed to compare the effects of repeated restraint stress alone and the combination with clomipramine treatment on parameters of oxidative stress in cerebral cortex, striatum and hippocampus of male rats. Animals were divided into control and repeated restraint stress, and subdivided into...
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Published in: | Neurochemical research 2010-11, Vol.35 (11), p.1761-1770 |
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container_title | Neurochemical research |
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creator | de Souza Balk, Rodrigo Bridi, Jessika Cristina de Lima Portella, Rafael Carvalho, Nelson Rodrigues Dobrachinski, Fernando da Silva, Michele Hinerasky Amaral, Guilherme Pires Dias, Glaecir Roseni Mundstock de Vargas Barbosa, Nilda Soares, Felix Alexandre Antunes |
description | This study aimed to compare the effects of repeated restraint stress alone and the combination with clomipramine treatment on parameters of oxidative stress in cerebral cortex, striatum and hippocampus of male rats. Animals were divided into control and repeated restraint stress, and subdivided into treated or not with clomipramine. After 40 days of stress and 27 days of clomipramine treatment with 30 mg/kg, the repeated restraint stress alone reduced levels of Na
+
, K
+
-ATPase in all tissues studied. The combination of repeated restraint stress and clomipramine increased the lipid peroxidation, free radicals and CAT activity as well as decreased levels of NP-SH in the tissues studied. However, Na
+
, K
+
-ATPase level decreased in striatum and cerebral cortex and the SOD activity increased in hippocampus and striatum. Results indicated that clomipramine may have deleterious effects on the central nervous system especially when associated with repeated restraint stress and chronically administered in non therapeutic levels. |
doi_str_mv | 10.1007/s11064-010-0240-1 |
format | article |
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+
, K
+
-ATPase in all tissues studied. The combination of repeated restraint stress and clomipramine increased the lipid peroxidation, free radicals and CAT activity as well as decreased levels of NP-SH in the tissues studied. However, Na
+
, K
+
-ATPase level decreased in striatum and cerebral cortex and the SOD activity increased in hippocampus and striatum. Results indicated that clomipramine may have deleterious effects on the central nervous system especially when associated with repeated restraint stress and chronically administered in non therapeutic levels.</description><identifier>ISSN: 0364-3190</identifier><identifier>EISSN: 1573-6903</identifier><identifier>DOI: 10.1007/s11064-010-0240-1</identifier><identifier>PMID: 20694755</identifier><language>eng</language><publisher>Boston: Springer US</publisher><subject>Animals ; Antioxidants - metabolism ; Biochemistry ; Biomedical and Life Sciences ; Biomedicine ; Brain - drug effects ; Brain - physiopathology ; Catalase - metabolism ; Cell Biology ; Clomipramine - pharmacology ; Lipid Peroxidation - drug effects ; Male ; Neurochemistry ; Neurology ; Neurosciences ; Original Paper ; Oxidative Stress - drug effects ; Rats ; Rats, Wistar ; Restraint, Physical ; Stress, Psychological - physiopathology ; Superoxide Dismutase - metabolism ; Thiobarbituric Acid Reactive Substances - metabolism</subject><ispartof>Neurochemical research, 2010-11, Vol.35 (11), p.1761-1770</ispartof><rights>Springer Science+Business Media, LLC 2010</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c402t-5882ed2a390d12ab44e1fe10dd8d39fd7efd9689878f28c59fb3ec08c59f1b463</citedby><cites>FETCH-LOGICAL-c402t-5882ed2a390d12ab44e1fe10dd8d39fd7efd9689878f28c59fb3ec08c59f1b463</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/20694755$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>de Souza Balk, Rodrigo</creatorcontrib><creatorcontrib>Bridi, Jessika Cristina</creatorcontrib><creatorcontrib>de Lima Portella, Rafael</creatorcontrib><creatorcontrib>Carvalho, Nelson Rodrigues</creatorcontrib><creatorcontrib>Dobrachinski, Fernando</creatorcontrib><creatorcontrib>da Silva, Michele Hinerasky</creatorcontrib><creatorcontrib>Amaral, Guilherme Pires</creatorcontrib><creatorcontrib>Dias, Glaecir Roseni Mundstock</creatorcontrib><creatorcontrib>de Vargas Barbosa, Nilda</creatorcontrib><creatorcontrib>Soares, Felix Alexandre Antunes</creatorcontrib><title>Clomipramine Treatment and Repeated Restraint Stress Alter Parameters of Oxidative Stress in Brain Regions of Male Rats</title><title>Neurochemical research</title><addtitle>Neurochem Res</addtitle><addtitle>Neurochem Res</addtitle><description>This study aimed to compare the effects of repeated restraint stress alone and the combination with clomipramine treatment on parameters of oxidative stress in cerebral cortex, striatum and hippocampus of male rats. Animals were divided into control and repeated restraint stress, and subdivided into treated or not with clomipramine. After 40 days of stress and 27 days of clomipramine treatment with 30 mg/kg, the repeated restraint stress alone reduced levels of Na
+
, K
+
-ATPase in all tissues studied. The combination of repeated restraint stress and clomipramine increased the lipid peroxidation, free radicals and CAT activity as well as decreased levels of NP-SH in the tissues studied. However, Na
+
, K
+
-ATPase level decreased in striatum and cerebral cortex and the SOD activity increased in hippocampus and striatum. Results indicated that clomipramine may have deleterious effects on the central nervous system especially when associated with repeated restraint stress and chronically administered in non therapeutic levels.</description><subject>Animals</subject><subject>Antioxidants - metabolism</subject><subject>Biochemistry</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Brain - drug effects</subject><subject>Brain - physiopathology</subject><subject>Catalase - metabolism</subject><subject>Cell Biology</subject><subject>Clomipramine - pharmacology</subject><subject>Lipid Peroxidation - drug effects</subject><subject>Male</subject><subject>Neurochemistry</subject><subject>Neurology</subject><subject>Neurosciences</subject><subject>Original Paper</subject><subject>Oxidative Stress - drug effects</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Restraint, Physical</subject><subject>Stress, Psychological - physiopathology</subject><subject>Superoxide Dismutase - 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metabolism</topic><topic>Biochemistry</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Brain - drug effects</topic><topic>Brain - physiopathology</topic><topic>Catalase - metabolism</topic><topic>Cell Biology</topic><topic>Clomipramine - pharmacology</topic><topic>Lipid Peroxidation - drug effects</topic><topic>Male</topic><topic>Neurochemistry</topic><topic>Neurology</topic><topic>Neurosciences</topic><topic>Original Paper</topic><topic>Oxidative Stress - drug effects</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>Restraint, Physical</topic><topic>Stress, Psychological - physiopathology</topic><topic>Superoxide Dismutase - metabolism</topic><topic>Thiobarbituric Acid Reactive Substances - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>de Souza Balk, Rodrigo</creatorcontrib><creatorcontrib>Bridi, Jessika Cristina</creatorcontrib><creatorcontrib>de Lima Portella, Rafael</creatorcontrib><creatorcontrib>Carvalho, Nelson Rodrigues</creatorcontrib><creatorcontrib>Dobrachinski, Fernando</creatorcontrib><creatorcontrib>da Silva, Michele Hinerasky</creatorcontrib><creatorcontrib>Amaral, Guilherme Pires</creatorcontrib><creatorcontrib>Dias, Glaecir Roseni Mundstock</creatorcontrib><creatorcontrib>de Vargas Barbosa, Nilda</creatorcontrib><creatorcontrib>Soares, Felix Alexandre Antunes</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>Chemoreception Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</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</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>AUTh Library subscriptions: ProQuest Central</collection><collection>ProQuest Natural Science Collection</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>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Biological Science Database</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>MEDLINE - Academic</collection><jtitle>Neurochemical research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>de Souza Balk, Rodrigo</au><au>Bridi, Jessika Cristina</au><au>de Lima Portella, Rafael</au><au>Carvalho, Nelson Rodrigues</au><au>Dobrachinski, Fernando</au><au>da Silva, Michele Hinerasky</au><au>Amaral, Guilherme Pires</au><au>Dias, Glaecir Roseni Mundstock</au><au>de Vargas Barbosa, Nilda</au><au>Soares, Felix Alexandre Antunes</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Clomipramine Treatment and Repeated Restraint Stress Alter Parameters of Oxidative Stress in Brain Regions of Male Rats</atitle><jtitle>Neurochemical research</jtitle><stitle>Neurochem Res</stitle><addtitle>Neurochem Res</addtitle><date>2010-11-01</date><risdate>2010</risdate><volume>35</volume><issue>11</issue><spage>1761</spage><epage>1770</epage><pages>1761-1770</pages><issn>0364-3190</issn><eissn>1573-6903</eissn><abstract>This study aimed to compare the effects of repeated restraint stress alone and the combination with clomipramine treatment on parameters of oxidative stress in cerebral cortex, striatum and hippocampus of male rats. Animals were divided into control and repeated restraint stress, and subdivided into treated or not with clomipramine. After 40 days of stress and 27 days of clomipramine treatment with 30 mg/kg, the repeated restraint stress alone reduced levels of Na
+
, K
+
-ATPase in all tissues studied. The combination of repeated restraint stress and clomipramine increased the lipid peroxidation, free radicals and CAT activity as well as decreased levels of NP-SH in the tissues studied. However, Na
+
, K
+
-ATPase level decreased in striatum and cerebral cortex and the SOD activity increased in hippocampus and striatum. Results indicated that clomipramine may have deleterious effects on the central nervous system especially when associated with repeated restraint stress and chronically administered in non therapeutic levels.</abstract><cop>Boston</cop><pub>Springer US</pub><pmid>20694755</pmid><doi>10.1007/s11064-010-0240-1</doi><tpages>10</tpages></addata></record> |
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subjects | Animals Antioxidants - metabolism Biochemistry Biomedical and Life Sciences Biomedicine Brain - drug effects Brain - physiopathology Catalase - metabolism Cell Biology Clomipramine - pharmacology Lipid Peroxidation - drug effects Male Neurochemistry Neurology Neurosciences Original Paper Oxidative Stress - drug effects Rats Rats, Wistar Restraint, Physical Stress, Psychological - physiopathology Superoxide Dismutase - metabolism Thiobarbituric Acid Reactive Substances - metabolism |
title | Clomipramine Treatment and Repeated Restraint Stress Alter Parameters of Oxidative Stress in Brain Regions of Male Rats |
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