Cytotoxic effects of autoxidative glycation
Incubation of the RNA phage Qβ at 37°C with a mixture of 100 mM ribose and 10 μM CuSO 4 resulted in a complete loss of viable phage after 20 min. This cytotoxic effect required both ribose and cupric ions. There was a direct correlation between the decrease in the percentage of phage survival and: (...
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Veröffentlicht in: | Free radical biology & medicine 1995-02, Vol.18 (2), p.265-269 |
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creator | Carubelli, Raoul Schneider, J.Edward Pye, Quentin N. Floyd, Robert A. |
description | Incubation of the RNA phage Qβ at 37°C with a mixture of 100 mM ribose and 10 μM CuSO
4 resulted in a complete loss of viable phage after 20 min. This cytotoxic effect required both ribose and cupric ions. There was a direct correlation between the decrease in the percentage of phage survival and: (a) the length of incubation, and (b) the concentrations of both ribose and CuSO
4. Addition of the strong chelator diethylenetriaminepentaacetic acid abolished the cytotoxic effect. These results are consistent with an initial production of superoxide free radicals by transition metal catalyzed autoxidation of ribose and Amadori products, followed by dismutation of superoxide to hydrogen peroxide and generation of lethal hydroxyl radicals by the Fenton reaction. RNA isolated from phage incubated with ribose and CuSO
4 retained its infectivity, suggesting that the cytotoxic effect may be mediated by a free radical attack on proteinaceous components of the phage through a site specific generation of hydroxyl radicals on protein-bound transition metal ions. |
doi_str_mv | 10.1016/0891-5849(94)E0134-5 |
format | Article |
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4 resulted in a complete loss of viable phage after 20 min. This cytotoxic effect required both ribose and cupric ions. There was a direct correlation between the decrease in the percentage of phage survival and: (a) the length of incubation, and (b) the concentrations of both ribose and CuSO
4. Addition of the strong chelator diethylenetriaminepentaacetic acid abolished the cytotoxic effect. These results are consistent with an initial production of superoxide free radicals by transition metal catalyzed autoxidation of ribose and Amadori products, followed by dismutation of superoxide to hydrogen peroxide and generation of lethal hydroxyl radicals by the Fenton reaction. RNA isolated from phage incubated with ribose and CuSO
4 retained its infectivity, suggesting that the cytotoxic effect may be mediated by a free radical attack on proteinaceous components of the phage through a site specific generation of hydroxyl radicals on protein-bound transition metal ions.</description><identifier>ISSN: 0891-5849</identifier><identifier>EISSN: 1873-4596</identifier><identifier>DOI: 10.1016/0891-5849(94)E0134-5</identifier><identifier>PMID: 7744310</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Autoxidation ; Copper - pharmacology ; Copper Sulfate ; CuSO 4 ; Cytotoxicity ; Free Radicals ; Glycation ; Glycosylation ; Hydrogen Peroxide - metabolism ; Hydroxyl Radical - metabolism ; Hydroxyl Radical - pharmacology ; Oxidation-Reduction ; Pentetic Acid - pharmacology ; Phage ; phage Q beta ; Ribose ; Ribose - pharmacology ; RNA Phages - drug effects ; Superoxides - metabolism ; Transition metals</subject><ispartof>Free radical biology & medicine, 1995-02, Vol.18 (2), p.265-269</ispartof><rights>1995</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c454t-dd1290f2e4b908a67c3a557f8fb7f9b89b3efeb300593617d2d018e1175f72ce3</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/0891-5849(94)E0134-5$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3536,27903,27904,45974</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/7744310$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Carubelli, Raoul</creatorcontrib><creatorcontrib>Schneider, J.Edward</creatorcontrib><creatorcontrib>Pye, Quentin N.</creatorcontrib><creatorcontrib>Floyd, Robert A.</creatorcontrib><title>Cytotoxic effects of autoxidative glycation</title><title>Free radical biology & medicine</title><addtitle>Free Radic Biol Med</addtitle><description>Incubation of the RNA phage Qβ at 37°C with a mixture of 100 mM ribose and 10 μM CuSO
4 resulted in a complete loss of viable phage after 20 min. This cytotoxic effect required both ribose and cupric ions. There was a direct correlation between the decrease in the percentage of phage survival and: (a) the length of incubation, and (b) the concentrations of both ribose and CuSO
4. Addition of the strong chelator diethylenetriaminepentaacetic acid abolished the cytotoxic effect. These results are consistent with an initial production of superoxide free radicals by transition metal catalyzed autoxidation of ribose and Amadori products, followed by dismutation of superoxide to hydrogen peroxide and generation of lethal hydroxyl radicals by the Fenton reaction. RNA isolated from phage incubated with ribose and CuSO
4 retained its infectivity, suggesting that the cytotoxic effect may be mediated by a free radical attack on proteinaceous components of the phage through a site specific generation of hydroxyl radicals on protein-bound transition metal ions.</description><subject>Autoxidation</subject><subject>Copper - pharmacology</subject><subject>Copper Sulfate</subject><subject>CuSO 4</subject><subject>Cytotoxicity</subject><subject>Free Radicals</subject><subject>Glycation</subject><subject>Glycosylation</subject><subject>Hydrogen Peroxide - metabolism</subject><subject>Hydroxyl Radical - metabolism</subject><subject>Hydroxyl Radical - pharmacology</subject><subject>Oxidation-Reduction</subject><subject>Pentetic Acid - pharmacology</subject><subject>Phage</subject><subject>phage Q beta</subject><subject>Ribose</subject><subject>Ribose - pharmacology</subject><subject>RNA Phages - drug effects</subject><subject>Superoxides - metabolism</subject><subject>Transition metals</subject><issn>0891-5849</issn><issn>1873-4596</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1995</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkE1LAzEQhoMotVb_gcKeRJHVZJNskosgpX5AwYueQzaZSGTb1M1usf_eXVt61NMM834MPAidE3xLMCnvsFQk55KpK8WuZ5hQlvMDNCZS0JxxVR6i8d5yjE5S-sQYM07lCI2EYIwSPEY3000b2_gdbAbeg21TFn1muuHkTBvWkH3UG9tvcXmKjrypE5zt5gS9P87eps_5_PXpZfowzy3jrM2dI4XCvgBWKSxNKSw1nAsvfSW8qqSqKHioKMZc0ZIIVzhMJBAiuBeFBTpBl9veVRO_OkitXoRkoa7NEmKXtBBFKQnH_xoJ71lwNhjZ1mibmFIDXq-asDDNRhOsB5h6IKUHUlox_QtT8z52sevvqgW4fWhHr9fvtzr0NNYBGp1sgKUFF5oepXYx_P3gB1etgo0</recordid><startdate>19950201</startdate><enddate>19950201</enddate><creator>Carubelli, Raoul</creator><creator>Schneider, J.Edward</creator><creator>Pye, Quentin N.</creator><creator>Floyd, Robert A.</creator><general>Elsevier Inc</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>7U9</scope><scope>H94</scope><scope>7X8</scope></search><sort><creationdate>19950201</creationdate><title>Cytotoxic effects of autoxidative glycation</title><author>Carubelli, Raoul ; Schneider, J.Edward ; Pye, Quentin N. ; Floyd, Robert A.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c454t-dd1290f2e4b908a67c3a557f8fb7f9b89b3efeb300593617d2d018e1175f72ce3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1995</creationdate><topic>Autoxidation</topic><topic>Copper - pharmacology</topic><topic>Copper Sulfate</topic><topic>CuSO 4</topic><topic>Cytotoxicity</topic><topic>Free Radicals</topic><topic>Glycation</topic><topic>Glycosylation</topic><topic>Hydrogen Peroxide - metabolism</topic><topic>Hydroxyl Radical - metabolism</topic><topic>Hydroxyl Radical - pharmacology</topic><topic>Oxidation-Reduction</topic><topic>Pentetic Acid - pharmacology</topic><topic>Phage</topic><topic>phage Q beta</topic><topic>Ribose</topic><topic>Ribose - pharmacology</topic><topic>RNA Phages - drug effects</topic><topic>Superoxides - metabolism</topic><topic>Transition metals</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Carubelli, Raoul</creatorcontrib><creatorcontrib>Schneider, J.Edward</creatorcontrib><creatorcontrib>Pye, Quentin N.</creatorcontrib><creatorcontrib>Floyd, Robert A.</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Virology and AIDS Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Free radical biology & medicine</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Carubelli, Raoul</au><au>Schneider, J.Edward</au><au>Pye, Quentin N.</au><au>Floyd, Robert A.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Cytotoxic effects of autoxidative glycation</atitle><jtitle>Free radical biology & medicine</jtitle><addtitle>Free Radic Biol Med</addtitle><date>1995-02-01</date><risdate>1995</risdate><volume>18</volume><issue>2</issue><spage>265</spage><epage>269</epage><pages>265-269</pages><issn>0891-5849</issn><eissn>1873-4596</eissn><abstract>Incubation of the RNA phage Qβ at 37°C with a mixture of 100 mM ribose and 10 μM CuSO
4 resulted in a complete loss of viable phage after 20 min. This cytotoxic effect required both ribose and cupric ions. There was a direct correlation between the decrease in the percentage of phage survival and: (a) the length of incubation, and (b) the concentrations of both ribose and CuSO
4. Addition of the strong chelator diethylenetriaminepentaacetic acid abolished the cytotoxic effect. These results are consistent with an initial production of superoxide free radicals by transition metal catalyzed autoxidation of ribose and Amadori products, followed by dismutation of superoxide to hydrogen peroxide and generation of lethal hydroxyl radicals by the Fenton reaction. RNA isolated from phage incubated with ribose and CuSO
4 retained its infectivity, suggesting that the cytotoxic effect may be mediated by a free radical attack on proteinaceous components of the phage through a site specific generation of hydroxyl radicals on protein-bound transition metal ions.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>7744310</pmid><doi>10.1016/0891-5849(94)E0134-5</doi><tpages>5</tpages></addata></record> |
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source | MEDLINE; Elsevier ScienceDirect Journals Complete |
subjects | Autoxidation Copper - pharmacology Copper Sulfate CuSO 4 Cytotoxicity Free Radicals Glycation Glycosylation Hydrogen Peroxide - metabolism Hydroxyl Radical - metabolism Hydroxyl Radical - pharmacology Oxidation-Reduction Pentetic Acid - pharmacology Phage phage Q beta Ribose Ribose - pharmacology RNA Phages - drug effects Superoxides - metabolism Transition metals |
title | Cytotoxic effects of autoxidative glycation |
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