Mitochondrial oxidative stress in female and male rat brain after ex vivo carbon monoxide treatment
Carbon monoxide (CO) is the most common cause of fatal poisoning all over the world. At the cellular level, a combination of tissue hypoxia and direct cellular damage underlie the pathophysiology of CO toxicity. The purpose of this study was to determine the effect of CO treatment on oxidative stres...
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description | Carbon monoxide (CO) is the most common cause of fatal poisoning all over the world. At the cellular level, a combination of tissue hypoxia and direct cellular damage underlie the pathophysiology of CO toxicity. The purpose of this study was to determine the effect of CO treatment on oxidative stress parameters in mitochondria isolated from male and female rat brains. Mitochondria prepared from frontal cortex, hippocampus and corpus striatum were treated with 0.1% CO at 37°C for 30 minutes; control samples were not exposed to CO. Cytochrome c oxidase activity (COX), lipid peroxidation (thiobarbituric acid reactive species = TBARS), protein oxidation (protein carbonyls) and glutathione (GSH) levels were measured in CO treated and control samples. Our results confirmed previous studies reporting the inhibition of cytochrome c oxidase activity by CO in rat brain. Additionally, protein carbonyl levels in the hippocampus and striatum significantly increased after CO treatment in male rats. While CO treatment caused a significant decrease in GSH levels in the cortex and striatum in male rats, reduced GSH levels were observed in the cortex and hippocampus in female rats following CO exposure. Taken together, our data suggest a role for mitochondrial oxidative stress in CO toxicity at the cellular level during CO poisoning.
Human & Experimental Toxicology (2007) 26,
645—651 |
doi_str_mv | 10.1177/0960327107076882 |
format | Article |
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Human & Experimental Toxicology (2007) 26,
645—651</description><identifier>ISSN: 0960-3271</identifier><identifier>EISSN: 1477-0903</identifier><identifier>DOI: 10.1177/0960327107076882</identifier><identifier>PMID: 17884952</identifier><language>eng</language><publisher>London, England: SAGE Publications</publisher><subject>Animals ; Biological and medical sciences ; Brain - drug effects ; Brain - enzymology ; Brain - metabolism ; Brain research ; Carbon monoxide ; Carbon Monoxide - toxicity ; Cellular biology ; Cerebral Cortex - drug effects ; Cerebral Cortex - metabolism ; Chemical and industrial products toxicology. Toxic occupational diseases ; Corpus Striatum - drug effects ; Corpus Striatum - metabolism ; Electron Transport Complex IV - metabolism ; Female ; Gas, fumes ; Glutathione - metabolism ; Hippocampus - drug effects ; Hippocampus - metabolism ; In Vitro Techniques ; Lipid Peroxidation - drug effects ; Male ; Medical sciences ; Mitochondria - drug effects ; Mitochondria - enzymology ; Mitochondria - metabolism ; Oxidation ; Oxidative Stress - drug effects ; Protein Carbonylation - drug effects ; Rats ; Rats, Sprague-Dawley ; Rodents ; Toxicology</subject><ispartof>Human & experimental toxicology, 2007-08, Vol.26 (8), p.645-651</ispartof><rights>2007 INIST-CNRS</rights><rights>SAGE Publications © Aug 2007</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c423t-44fe29a4ec97500475d3c9689620b4620beb14df6554f8c3d15786f525ea2acd3</citedby><cites>FETCH-LOGICAL-c423t-44fe29a4ec97500475d3c9689620b4620beb14df6554f8c3d15786f525ea2acd3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://journals.sagepub.com/doi/pdf/10.1177/0960327107076882$$EPDF$$P50$$Gsage$$H</linktopdf><linktohtml>$$Uhttps://journals.sagepub.com/doi/10.1177/0960327107076882$$EHTML$$P50$$Gsage$$H</linktohtml><link.rule.ids>314,777,781,21947,27834,27905,27906,44926,45314</link.rule.ids><linktorsrc>$$Uhttps://journals.sagepub.com/doi/full/10.1177/0960327107076882?utm_source=summon&utm_medium=discovery-provider$$EView_record_in_SAGE_Publications$$FView_record_in_$$GSAGE_Publications</linktorsrc><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=19110594$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17884952$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Taskiran, D.</creatorcontrib><creatorcontrib>Nesil, T.</creatorcontrib><creatorcontrib>Alkan, K.</creatorcontrib><title>Mitochondrial oxidative stress in female and male rat brain after ex vivo carbon monoxide treatment</title><title>Human & experimental toxicology</title><addtitle>Hum Exp Toxicol</addtitle><description>Carbon monoxide (CO) is the most common cause of fatal poisoning all over the world. At the cellular level, a combination of tissue hypoxia and direct cellular damage underlie the pathophysiology of CO toxicity. The purpose of this study was to determine the effect of CO treatment on oxidative stress parameters in mitochondria isolated from male and female rat brains. Mitochondria prepared from frontal cortex, hippocampus and corpus striatum were treated with 0.1% CO at 37°C for 30 minutes; control samples were not exposed to CO. Cytochrome c oxidase activity (COX), lipid peroxidation (thiobarbituric acid reactive species = TBARS), protein oxidation (protein carbonyls) and glutathione (GSH) levels were measured in CO treated and control samples. Our results confirmed previous studies reporting the inhibition of cytochrome c oxidase activity by CO in rat brain. Additionally, protein carbonyl levels in the hippocampus and striatum significantly increased after CO treatment in male rats. While CO treatment caused a significant decrease in GSH levels in the cortex and striatum in male rats, reduced GSH levels were observed in the cortex and hippocampus in female rats following CO exposure. Taken together, our data suggest a role for mitochondrial oxidative stress in CO toxicity at the cellular level during CO poisoning.
Human & Experimental Toxicology (2007) 26,
645—651</description><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Brain - drug effects</subject><subject>Brain - enzymology</subject><subject>Brain - metabolism</subject><subject>Brain research</subject><subject>Carbon monoxide</subject><subject>Carbon Monoxide - toxicity</subject><subject>Cellular biology</subject><subject>Cerebral Cortex - drug effects</subject><subject>Cerebral Cortex - metabolism</subject><subject>Chemical and industrial products toxicology. Toxic occupational diseases</subject><subject>Corpus Striatum - drug effects</subject><subject>Corpus Striatum - metabolism</subject><subject>Electron Transport Complex IV - metabolism</subject><subject>Female</subject><subject>Gas, fumes</subject><subject>Glutathione - metabolism</subject><subject>Hippocampus - drug effects</subject><subject>Hippocampus - metabolism</subject><subject>In Vitro Techniques</subject><subject>Lipid Peroxidation - drug effects</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Mitochondria - drug effects</subject><subject>Mitochondria - enzymology</subject><subject>Mitochondria - metabolism</subject><subject>Oxidation</subject><subject>Oxidative Stress - drug effects</subject><subject>Protein Carbonylation - drug effects</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Rodents</subject><subject>Toxicology</subject><issn>0960-3271</issn><issn>1477-0903</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2007</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNp1kM2LFDEQxYMo7rh69yRB0Ftrks7nUZb1A1a86LmpTlc0S3eyJplh_e_tdgYGFrxUFbxfvSoeIS85e8e5Me-Z06wXhjPDjLZWPCI7Lo3pmGP9Y7Lb5G7TL8izWm8ZY9op_pRccGOtdErsiP8aW_a_cppKhJnm-zhBiwektRWslcZEAy4wI4U00X9DgUbHAqsCoWGheE8P8ZCphzLmRJecNhekqwG0BVN7Tp4EmCu-OPVL8uPj9ferz93Nt09frj7cdF6KvnVSBhQOJHpnFGPSqKn3TlunBRvlVnDkcgpaKRms7yeujNVBCYUgwE_9JXl79L0r-fceaxuWWD3OMyTM-zoI1muhuF3B1w_A27wvaf1tEIJZLrQVK8SOkC-51oJhuCtxgfJn4GzY0h8epr-uvDr57scFp_PCKe4VeHMCoHqYQ4HkYz1zjnOmnFy57shV-Inn5_57-C-TWpjQ</recordid><startdate>20070801</startdate><enddate>20070801</enddate><creator>Taskiran, D.</creator><creator>Nesil, T.</creator><creator>Alkan, K.</creator><general>SAGE Publications</general><general>Arnold</general><general>Sage Publications Ltd</general><scope>IQODW</scope><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>7RV</scope><scope>7ST</scope><scope>7TK</scope><scope>7U7</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>C1K</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>KB0</scope><scope>M0S</scope><scope>M1P</scope><scope>NAPCQ</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>SOI</scope></search><sort><creationdate>20070801</creationdate><title>Mitochondrial oxidative stress in female and male rat brain after ex vivo carbon monoxide treatment</title><author>Taskiran, D. ; Nesil, T. ; Alkan, K.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c423t-44fe29a4ec97500475d3c9689620b4620beb14df6554f8c3d15786f525ea2acd3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2007</creationdate><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Brain - drug effects</topic><topic>Brain - enzymology</topic><topic>Brain - metabolism</topic><topic>Brain research</topic><topic>Carbon monoxide</topic><topic>Carbon Monoxide - toxicity</topic><topic>Cellular biology</topic><topic>Cerebral Cortex - drug effects</topic><topic>Cerebral Cortex - metabolism</topic><topic>Chemical and industrial products toxicology. Toxic occupational diseases</topic><topic>Corpus Striatum - drug effects</topic><topic>Corpus Striatum - metabolism</topic><topic>Electron Transport Complex IV - metabolism</topic><topic>Female</topic><topic>Gas, fumes</topic><topic>Glutathione - metabolism</topic><topic>Hippocampus - drug effects</topic><topic>Hippocampus - metabolism</topic><topic>In Vitro Techniques</topic><topic>Lipid Peroxidation - drug effects</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Mitochondria - drug effects</topic><topic>Mitochondria - enzymology</topic><topic>Mitochondria - metabolism</topic><topic>Oxidation</topic><topic>Oxidative Stress - drug effects</topic><topic>Protein Carbonylation - drug effects</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Rodents</topic><topic>Toxicology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Taskiran, D.</creatorcontrib><creatorcontrib>Nesil, T.</creatorcontrib><creatorcontrib>Alkan, K.</creatorcontrib><collection>Pascal-Francis</collection><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>Nursing & Allied Health Database</collection><collection>Environment Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</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 Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Nursing & Allied Health Premium</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>Environment Abstracts</collection><jtitle>Human & experimental toxicology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext_linktorsrc</fulltext></delivery><addata><au>Taskiran, D.</au><au>Nesil, T.</au><au>Alkan, K.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Mitochondrial oxidative stress in female and male rat brain after ex vivo carbon monoxide treatment</atitle><jtitle>Human & experimental toxicology</jtitle><addtitle>Hum Exp Toxicol</addtitle><date>2007-08-01</date><risdate>2007</risdate><volume>26</volume><issue>8</issue><spage>645</spage><epage>651</epage><pages>645-651</pages><issn>0960-3271</issn><eissn>1477-0903</eissn><abstract>Carbon monoxide (CO) is the most common cause of fatal poisoning all over the world. At the cellular level, a combination of tissue hypoxia and direct cellular damage underlie the pathophysiology of CO toxicity. The purpose of this study was to determine the effect of CO treatment on oxidative stress parameters in mitochondria isolated from male and female rat brains. Mitochondria prepared from frontal cortex, hippocampus and corpus striatum were treated with 0.1% CO at 37°C for 30 minutes; control samples were not exposed to CO. Cytochrome c oxidase activity (COX), lipid peroxidation (thiobarbituric acid reactive species = TBARS), protein oxidation (protein carbonyls) and glutathione (GSH) levels were measured in CO treated and control samples. Our results confirmed previous studies reporting the inhibition of cytochrome c oxidase activity by CO in rat brain. Additionally, protein carbonyl levels in the hippocampus and striatum significantly increased after CO treatment in male rats. While CO treatment caused a significant decrease in GSH levels in the cortex and striatum in male rats, reduced GSH levels were observed in the cortex and hippocampus in female rats following CO exposure. Taken together, our data suggest a role for mitochondrial oxidative stress in CO toxicity at the cellular level during CO poisoning.
Human & Experimental Toxicology (2007) 26,
645—651</abstract><cop>London, England</cop><pub>SAGE Publications</pub><pmid>17884952</pmid><doi>10.1177/0960327107076882</doi><tpages>7</tpages></addata></record> |
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subjects | Animals Biological and medical sciences Brain - drug effects Brain - enzymology Brain - metabolism Brain research Carbon monoxide Carbon Monoxide - toxicity Cellular biology Cerebral Cortex - drug effects Cerebral Cortex - metabolism Chemical and industrial products toxicology. Toxic occupational diseases Corpus Striatum - drug effects Corpus Striatum - metabolism Electron Transport Complex IV - metabolism Female Gas, fumes Glutathione - metabolism Hippocampus - drug effects Hippocampus - metabolism In Vitro Techniques Lipid Peroxidation - drug effects Male Medical sciences Mitochondria - drug effects Mitochondria - enzymology Mitochondria - metabolism Oxidation Oxidative Stress - drug effects Protein Carbonylation - drug effects Rats Rats, Sprague-Dawley Rodents Toxicology |
title | Mitochondrial oxidative stress in female and male rat brain after ex vivo carbon monoxide treatment |
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