Quercitrin, a glycoside form of quercetin, prevents lipid peroxidation in vitro
Reactive oxygen species have been demonstrated to be associated with a variety of diseases including neurodegenerative disorders. Flavonoid compounds have been investigated for their protective action against oxidative mechanisms in different in vivo and in vitro models, which seems to be linked to...
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| Veröffentlicht in: | Brain research 2006-08, Vol.1107 (1), p.192-198 |
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| creator | Wagner, Caroline Fachinetto, Roselei Dalla Corte, Cristiane Lenz Brito, Verônica Bidinotto Severo, Diego de Oliveira Costa Dias, Gilvan Morel, Ademir F. Nogueira, Cristina W. Rocha, João B.T. |
| description | Reactive oxygen species have been demonstrated to be associated with a variety of diseases including neurodegenerative disorders. Flavonoid compounds have been investigated for their protective action against oxidative mechanisms in different in vivo and in vitro models, which seems to be linked to their antioxidant properties. In the present study, we examine the protective mechanism of quercitrin, a glycoside form of quercetin, against the production of TBARS induced by different agents. TBARS production was stimulated by the incubation of rat brain homogenate with Fe
2+, Fe
2+ plus EDTA, quinolinic acid (QA), sodium nitroprusside (SNP) and potassium ferricyanide ([Fe(CN)
6]
3−). Quercitrin was able to prevent the formation of TBARS induced by pro-oxidant agents tested; however, it was more effective against potassium ferricyanide ([Fe(CN)
6]
3−, IC
50 = 2.5), than quinolinic acid (QA, IC
50 = 6 μg/ml) and sodium nitroprusside (SNP, IC
50 = 5.88 μg/ml) than Fe
2+ (Fe
2+, IC
50 = 14.81 μg/ml), Fe
2+ plus EDTA (Fe
2+ plus EDTA, IC
50 = 48.15 μg/ml). The effect of quercitrin on the Fenton reaction was also investigated (deoxyribose degradation). Quercitrin caused a significant decrease in deoxyribose degradation that was not dependent on the concentration. Taken together, the data presented here indicate that quercitrin exhibits a scavenger and antioxidant role, and these effects probably are mediated via different mechanisms, which may involve the negative modulation of the Fenton reaction and NMDA receptor. |
| doi_str_mv | 10.1016/j.brainres.2006.05.084 |
| format | Article |
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2+, Fe
2+ plus EDTA, quinolinic acid (QA), sodium nitroprusside (SNP) and potassium ferricyanide ([Fe(CN)
6]
3−). Quercitrin was able to prevent the formation of TBARS induced by pro-oxidant agents tested; however, it was more effective against potassium ferricyanide ([Fe(CN)
6]
3−, IC
50 = 2.5), than quinolinic acid (QA, IC
50 = 6 μg/ml) and sodium nitroprusside (SNP, IC
50 = 5.88 μg/ml) than Fe
2+ (Fe
2+, IC
50 = 14.81 μg/ml), Fe
2+ plus EDTA (Fe
2+ plus EDTA, IC
50 = 48.15 μg/ml). The effect of quercitrin on the Fenton reaction was also investigated (deoxyribose degradation). Quercitrin caused a significant decrease in deoxyribose degradation that was not dependent on the concentration. Taken together, the data presented here indicate that quercitrin exhibits a scavenger and antioxidant role, and these effects probably are mediated via different mechanisms, which may involve the negative modulation of the Fenton reaction and NMDA receptor.</description><identifier>ISSN: 0006-8993</identifier><identifier>EISSN: 1872-6240</identifier><identifier>DOI: 10.1016/j.brainres.2006.05.084</identifier><identifier>PMID: 16828712</identifier><identifier>CODEN: BRREAP</identifier><language>eng</language><publisher>London: Elsevier B.V</publisher><subject>Analysis of Variance ; Animals ; Antioxidants - pharmacology ; Biochemistry and metabolism ; Biological and medical sciences ; Brain - drug effects ; Central nervous system ; Deoxyribose degradation ; Dose-Response Relationship, Drug ; Drug Interactions ; Fenton reaction ; Flavonoids ; Fundamental and applied biological sciences. Psychology ; In Vitro Techniques ; Lipid Peroxidation - drug effects ; Male ; Neurotoxins - toxicity ; Oxidative stress ; Quercetin - analogs & derivatives ; Quercetin - chemistry ; Quercetin - pharmacology ; Quercitrin ; Quinolinic acid ; Rats ; Rats, Wistar ; Sodium nitroprusside ; TBARS ; Thiobarbituric Acid Reactive Substances - metabolism ; Vertebrates: nervous system and sense organs</subject><ispartof>Brain research, 2006-08, Vol.1107 (1), p.192-198</ispartof><rights>2006 Elsevier B.V.</rights><rights>2006 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c497t-2ed85901ed19c43313295ee85b7cfbdcc6f23032ceaa4f03e396ca779dccf9443</citedby><cites>FETCH-LOGICAL-c497t-2ed85901ed19c43313295ee85b7cfbdcc6f23032ceaa4f03e396ca779dccf9443</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.brainres.2006.05.084$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3550,27924,27925,45995</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=18051372$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/16828712$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wagner, Caroline</creatorcontrib><creatorcontrib>Fachinetto, Roselei</creatorcontrib><creatorcontrib>Dalla Corte, Cristiane Lenz</creatorcontrib><creatorcontrib>Brito, Verônica Bidinotto</creatorcontrib><creatorcontrib>Severo, Diego</creatorcontrib><creatorcontrib>de Oliveira Costa Dias, Gilvan</creatorcontrib><creatorcontrib>Morel, Ademir F.</creatorcontrib><creatorcontrib>Nogueira, Cristina W.</creatorcontrib><creatorcontrib>Rocha, João B.T.</creatorcontrib><title>Quercitrin, a glycoside form of quercetin, prevents lipid peroxidation in vitro</title><title>Brain research</title><addtitle>Brain Res</addtitle><description>Reactive oxygen species have been demonstrated to be associated with a variety of diseases including neurodegenerative disorders. Flavonoid compounds have been investigated for their protective action against oxidative mechanisms in different in vivo and in vitro models, which seems to be linked to their antioxidant properties. In the present study, we examine the protective mechanism of quercitrin, a glycoside form of quercetin, against the production of TBARS induced by different agents. TBARS production was stimulated by the incubation of rat brain homogenate with Fe
2+, Fe
2+ plus EDTA, quinolinic acid (QA), sodium nitroprusside (SNP) and potassium ferricyanide ([Fe(CN)
6]
3−). Quercitrin was able to prevent the formation of TBARS induced by pro-oxidant agents tested; however, it was more effective against potassium ferricyanide ([Fe(CN)
6]
3−, IC
50 = 2.5), than quinolinic acid (QA, IC
50 = 6 μg/ml) and sodium nitroprusside (SNP, IC
50 = 5.88 μg/ml) than Fe
2+ (Fe
2+, IC
50 = 14.81 μg/ml), Fe
2+ plus EDTA (Fe
2+ plus EDTA, IC
50 = 48.15 μg/ml). The effect of quercitrin on the Fenton reaction was also investigated (deoxyribose degradation). Quercitrin caused a significant decrease in deoxyribose degradation that was not dependent on the concentration. Taken together, the data presented here indicate that quercitrin exhibits a scavenger and antioxidant role, and these effects probably are mediated via different mechanisms, which may involve the negative modulation of the Fenton reaction and NMDA receptor.</description><subject>Analysis of Variance</subject><subject>Animals</subject><subject>Antioxidants - pharmacology</subject><subject>Biochemistry and metabolism</subject><subject>Biological and medical sciences</subject><subject>Brain - drug effects</subject><subject>Central nervous system</subject><subject>Deoxyribose degradation</subject><subject>Dose-Response Relationship, Drug</subject><subject>Drug Interactions</subject><subject>Fenton reaction</subject><subject>Flavonoids</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>In Vitro Techniques</subject><subject>Lipid Peroxidation - drug effects</subject><subject>Male</subject><subject>Neurotoxins - toxicity</subject><subject>Oxidative stress</subject><subject>Quercetin - analogs & derivatives</subject><subject>Quercetin - chemistry</subject><subject>Quercetin - pharmacology</subject><subject>Quercitrin</subject><subject>Quinolinic acid</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Sodium nitroprusside</subject><subject>TBARS</subject><subject>Thiobarbituric Acid Reactive Substances - metabolism</subject><subject>Vertebrates: nervous system and sense organs</subject><issn>0006-8993</issn><issn>1872-6240</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2006</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkE1LAzEQhoMoWqt_QXLRk7vmY79yU4pfUBBBzyFNJpKy3azJtui_N0tXPHqZMLzPTIYHoQtKckpodbPOV0G5LkDMGSFVTsqcNMUBmtGmZlnFCnKIZiQlWSMEP0GnMa5Ty7kgx-iEVg1raspm6OV1C0G7IbjuGiv80X5rH50BbH3YYG_x55jDMMZ9gB10Q8St653BPQT_5YwanO-w6_AubfFn6MiqNsL59M7R-8P92-IpW748Pi_ulpkuRD1kDExTCkLBUKELzilnogRoylWt7cpoXVnGCWcalCos4cBFpVVdixRZURR8jq72e_vg04lxkBsXNbSt6sBvo6SCF7xKdY6qPaiDjzGAlX1wGxW-JSVyVCnX8lelHFVKUsqkMg1eTD9sVxswf2OTuwRcToCKWrU2qE67-Mc1pKS8HrnbPQfJx85BkFE76DQYF0AP0nj33y0_xyuWnw</recordid><startdate>20060830</startdate><enddate>20060830</enddate><creator>Wagner, Caroline</creator><creator>Fachinetto, Roselei</creator><creator>Dalla Corte, Cristiane Lenz</creator><creator>Brito, Verônica Bidinotto</creator><creator>Severo, Diego</creator><creator>de Oliveira Costa Dias, Gilvan</creator><creator>Morel, Ademir F.</creator><creator>Nogueira, Cristina W.</creator><creator>Rocha, João B.T.</creator><general>Elsevier B.V</general><general>Elsevier</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>7TK</scope></search><sort><creationdate>20060830</creationdate><title>Quercitrin, a glycoside form of quercetin, prevents lipid peroxidation in vitro</title><author>Wagner, Caroline ; Fachinetto, Roselei ; Dalla Corte, Cristiane Lenz ; Brito, Verônica Bidinotto ; Severo, Diego ; de Oliveira Costa Dias, Gilvan ; Morel, Ademir F. ; Nogueira, Cristina W. ; Rocha, João B.T.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c497t-2ed85901ed19c43313295ee85b7cfbdcc6f23032ceaa4f03e396ca779dccf9443</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2006</creationdate><topic>Analysis of Variance</topic><topic>Animals</topic><topic>Antioxidants - pharmacology</topic><topic>Biochemistry and metabolism</topic><topic>Biological and medical sciences</topic><topic>Brain - drug effects</topic><topic>Central nervous system</topic><topic>Deoxyribose degradation</topic><topic>Dose-Response Relationship, Drug</topic><topic>Drug Interactions</topic><topic>Fenton reaction</topic><topic>Flavonoids</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>In Vitro Techniques</topic><topic>Lipid Peroxidation - drug effects</topic><topic>Male</topic><topic>Neurotoxins - toxicity</topic><topic>Oxidative stress</topic><topic>Quercetin - analogs & derivatives</topic><topic>Quercetin - chemistry</topic><topic>Quercetin - pharmacology</topic><topic>Quercitrin</topic><topic>Quinolinic acid</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>Sodium nitroprusside</topic><topic>TBARS</topic><topic>Thiobarbituric Acid Reactive Substances - metabolism</topic><topic>Vertebrates: nervous system and sense organs</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Wagner, Caroline</creatorcontrib><creatorcontrib>Fachinetto, Roselei</creatorcontrib><creatorcontrib>Dalla Corte, Cristiane Lenz</creatorcontrib><creatorcontrib>Brito, Verônica Bidinotto</creatorcontrib><creatorcontrib>Severo, Diego</creatorcontrib><creatorcontrib>de Oliveira Costa Dias, Gilvan</creatorcontrib><creatorcontrib>Morel, Ademir F.</creatorcontrib><creatorcontrib>Nogueira, Cristina W.</creatorcontrib><creatorcontrib>Rocha, João B.T.</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>Neurosciences Abstracts</collection><jtitle>Brain research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wagner, Caroline</au><au>Fachinetto, Roselei</au><au>Dalla Corte, Cristiane Lenz</au><au>Brito, Verônica Bidinotto</au><au>Severo, Diego</au><au>de Oliveira Costa Dias, Gilvan</au><au>Morel, Ademir F.</au><au>Nogueira, Cristina W.</au><au>Rocha, João B.T.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Quercitrin, a glycoside form of quercetin, prevents lipid peroxidation in vitro</atitle><jtitle>Brain research</jtitle><addtitle>Brain Res</addtitle><date>2006-08-30</date><risdate>2006</risdate><volume>1107</volume><issue>1</issue><spage>192</spage><epage>198</epage><pages>192-198</pages><issn>0006-8993</issn><eissn>1872-6240</eissn><coden>BRREAP</coden><abstract>Reactive oxygen species have been demonstrated to be associated with a variety of diseases including neurodegenerative disorders. Flavonoid compounds have been investigated for their protective action against oxidative mechanisms in different in vivo and in vitro models, which seems to be linked to their antioxidant properties. In the present study, we examine the protective mechanism of quercitrin, a glycoside form of quercetin, against the production of TBARS induced by different agents. TBARS production was stimulated by the incubation of rat brain homogenate with Fe
2+, Fe
2+ plus EDTA, quinolinic acid (QA), sodium nitroprusside (SNP) and potassium ferricyanide ([Fe(CN)
6]
3−). Quercitrin was able to prevent the formation of TBARS induced by pro-oxidant agents tested; however, it was more effective against potassium ferricyanide ([Fe(CN)
6]
3−, IC
50 = 2.5), than quinolinic acid (QA, IC
50 = 6 μg/ml) and sodium nitroprusside (SNP, IC
50 = 5.88 μg/ml) than Fe
2+ (Fe
2+, IC
50 = 14.81 μg/ml), Fe
2+ plus EDTA (Fe
2+ plus EDTA, IC
50 = 48.15 μg/ml). The effect of quercitrin on the Fenton reaction was also investigated (deoxyribose degradation). Quercitrin caused a significant decrease in deoxyribose degradation that was not dependent on the concentration. Taken together, the data presented here indicate that quercitrin exhibits a scavenger and antioxidant role, and these effects probably are mediated via different mechanisms, which may involve the negative modulation of the Fenton reaction and NMDA receptor.</abstract><cop>London</cop><cop>Amsterdam</cop><cop>New York, NY</cop><pub>Elsevier B.V</pub><pmid>16828712</pmid><doi>10.1016/j.brainres.2006.05.084</doi><tpages>7</tpages></addata></record> |
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| subjects | Analysis of Variance Animals Antioxidants - pharmacology Biochemistry and metabolism Biological and medical sciences Brain - drug effects Central nervous system Deoxyribose degradation Dose-Response Relationship, Drug Drug Interactions Fenton reaction Flavonoids Fundamental and applied biological sciences. Psychology In Vitro Techniques Lipid Peroxidation - drug effects Male Neurotoxins - toxicity Oxidative stress Quercetin - analogs & derivatives Quercetin - chemistry Quercetin - pharmacology Quercitrin Quinolinic acid Rats Rats, Wistar Sodium nitroprusside TBARS Thiobarbituric Acid Reactive Substances - metabolism Vertebrates: nervous system and sense organs |
| title | Quercitrin, a glycoside form of quercetin, prevents lipid peroxidation in vitro |
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