Induction of micronuclei in mouse and rat by glycidamide, genotoxic metabolite of acrylamide
Male CBA mice and male Sprague–Dawley rats were treated by i.p. injection of glycidamide (GA), the presumed genotoxic metabolite of acrylamide (AA). GA was obtained through a new way of synthesis. As an endpoint of chromosome damage, micronucleus (MN) induction in erythrocytes was measured. Hemoglob...
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| Veröffentlicht in: | Mutation research 2003-02, Vol.535 (1), p.15-24 |
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| creator | Paulsson, Birgit Kotova, Natalia Grawé, Jan Henderson, Alistair Granath, Fredrik Golding, Bernard Törnqvist, Margareta |
| description | Male CBA mice and male Sprague–Dawley rats were treated by i.p. injection of glycidamide (GA), the presumed genotoxic metabolite of acrylamide (AA). GA was obtained through a new way of synthesis. As an endpoint of chromosome damage, micronucleus (MN) induction in erythrocytes was measured. Hemoglobin (Hb) adducts were used as a measure of in vivo dose of GA. GA induced linear dose-dependent increases in adduct levels in both species. Rats exhibit, compared with mice, 30% higher Hb adduct levels per unit of administered amount of GA. The incremental MN frequencies per administered dose of GA in mice showed a linear-quadratic dose-dependent curve. In the rat no positive dose–response relationship was obtained, probably due to toxic effects to the bone marrow. The main result of this study is the finding that after treatment with synthetic GA the MN frequency per unit of the in vivo dose of GA in the mouse is very similar to that obtained in a previous study, where animals were treated with AA and GA as a metabolite. This equality in potency of GA, whether its in vivo dose is established by injection of synthetic GA or through metabolism of AA, supports the view that GA is the predominant genotoxic factor in AA exposure. |
| doi_str_mv | 10.1016/S1383-5718(02)00281-4 |
| format | Article |
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GA was obtained through a new way of synthesis. As an endpoint of chromosome damage, micronucleus (MN) induction in erythrocytes was measured. Hemoglobin (Hb) adducts were used as a measure of in vivo dose of GA. GA induced linear dose-dependent increases in adduct levels in both species. Rats exhibit, compared with mice, 30% higher Hb adduct levels per unit of administered amount of GA. The incremental MN frequencies per administered dose of GA in mice showed a linear-quadratic dose-dependent curve. In the rat no positive dose–response relationship was obtained, probably due to toxic effects to the bone marrow. The main result of this study is the finding that after treatment with synthetic GA the MN frequency per unit of the in vivo dose of GA in the mouse is very similar to that obtained in a previous study, where animals were treated with AA and GA as a metabolite. This equality in potency of GA, whether its in vivo dose is established by injection of synthetic GA or through metabolism of AA, supports the view that GA is the predominant genotoxic factor in AA exposure.</description><identifier>ISSN: 1383-5718</identifier><identifier>ISSN: 0027-5107</identifier><identifier>EISSN: 1879-3592</identifier><identifier>DOI: 10.1016/S1383-5718(02)00281-4</identifier><identifier>PMID: 12547279</identifier><language>eng</language><publisher>Amsterdam: Elsevier B.V</publisher><subject>Acrylamide ; Acrylamide - administration & dosage ; Acrylamide - metabolism ; Acrylamide - toxicity ; Animals ; Biological and medical sciences ; Carcinogenic ; Chemical mutagenesis ; Dose-Response Relationship, Drug ; Epoxy Compounds - administration & dosage ; Epoxy Compounds - metabolism ; Epoxy Compounds - toxicity ; Erythrocytes - drug effects ; Erythrocytes - metabolism ; Erythrocytes - ultrastructure ; Fundamental and applied biological sciences. Psychology ; Glycidamide ; Hemoglobin adducts ; Hemoglobins - chemistry ; Hemoglobins - drug effects ; Male ; Medical sciences ; Mice ; Mice, Inbred CBA ; Micronuclei ; Micronuclei, Chromosome-Defective - drug effects ; Micronucleus Tests ; Molecular and cellular biology ; Molecular genetics ; Mutagenesis. Repair ; Mutagens - administration & dosage ; Mutagens - toxicity ; Rats ; Rats, Sprague-Dawley ; Toxicology</subject><ispartof>Mutation research, 2003-02, Vol.535 (1), p.15-24</ispartof><rights>2002 Elsevier Science B.V.</rights><rights>2003 INIST-CNRS</rights><rights>Copyright 2002 Elsevier Science B.V.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c460t-5fd90d61f7586297793b899dd2dc71a1104cafd09abaa1bfea94b407827db5053</citedby><cites>FETCH-LOGICAL-c460t-5fd90d61f7586297793b899dd2dc71a1104cafd09abaa1bfea94b407827db5053</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S1383571802002814$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>230,314,776,780,881,3537,27901,27902,65534</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=14466836$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/12547279$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttp://kipublications.ki.se/Default.aspx?queryparsed=id:1943672$$DView record from Swedish Publication Index$$Hfree_for_read</backlink></links><search><creatorcontrib>Paulsson, Birgit</creatorcontrib><creatorcontrib>Kotova, Natalia</creatorcontrib><creatorcontrib>Grawé, Jan</creatorcontrib><creatorcontrib>Henderson, Alistair</creatorcontrib><creatorcontrib>Granath, Fredrik</creatorcontrib><creatorcontrib>Golding, Bernard</creatorcontrib><creatorcontrib>Törnqvist, Margareta</creatorcontrib><title>Induction of micronuclei in mouse and rat by glycidamide, genotoxic metabolite of acrylamide</title><title>Mutation research</title><addtitle>Mutat Res</addtitle><description>Male CBA mice and male Sprague–Dawley rats were treated by i.p. injection of glycidamide (GA), the presumed genotoxic metabolite of acrylamide (AA). GA was obtained through a new way of synthesis. As an endpoint of chromosome damage, micronucleus (MN) induction in erythrocytes was measured. Hemoglobin (Hb) adducts were used as a measure of in vivo dose of GA. GA induced linear dose-dependent increases in adduct levels in both species. Rats exhibit, compared with mice, 30% higher Hb adduct levels per unit of administered amount of GA. The incremental MN frequencies per administered dose of GA in mice showed a linear-quadratic dose-dependent curve. In the rat no positive dose–response relationship was obtained, probably due to toxic effects to the bone marrow. The main result of this study is the finding that after treatment with synthetic GA the MN frequency per unit of the in vivo dose of GA in the mouse is very similar to that obtained in a previous study, where animals were treated with AA and GA as a metabolite. This equality in potency of GA, whether its in vivo dose is established by injection of synthetic GA or through metabolism of AA, supports the view that GA is the predominant genotoxic factor in AA exposure.</description><subject>Acrylamide</subject><subject>Acrylamide - administration & dosage</subject><subject>Acrylamide - metabolism</subject><subject>Acrylamide - toxicity</subject><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Carcinogenic</subject><subject>Chemical mutagenesis</subject><subject>Dose-Response Relationship, Drug</subject><subject>Epoxy Compounds - administration & dosage</subject><subject>Epoxy Compounds - metabolism</subject><subject>Epoxy Compounds - toxicity</subject><subject>Erythrocytes - drug effects</subject><subject>Erythrocytes - metabolism</subject><subject>Erythrocytes - ultrastructure</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Glycidamide</subject><subject>Hemoglobin adducts</subject><subject>Hemoglobins - chemistry</subject><subject>Hemoglobins - drug effects</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Mice</subject><subject>Mice, Inbred CBA</subject><subject>Micronuclei</subject><subject>Micronuclei, Chromosome-Defective - drug effects</subject><subject>Micronucleus Tests</subject><subject>Molecular and cellular biology</subject><subject>Molecular genetics</subject><subject>Mutagenesis. Repair</subject><subject>Mutagens - administration & dosage</subject><subject>Mutagens - toxicity</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Toxicology</subject><issn>1383-5718</issn><issn>0027-5107</issn><issn>1879-3592</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2003</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkUtv1TAQhSMEog_4CSBvQCARsB07tlcVqkqpVKkLYIdk-TGpDIl9sZPC_ff1vTfQJasZjb45Y5_TNC8Ifk8w6T98IZ3sWi6IfIPpW4ypJC171BwTKVTbcUUf1_4vctSclPKjQrjD8mlzRChnggp13Hy_in5xc0gRpQFNweUUFzdCQCGiKS0FkIkeZTMju0W349YFb6bg4R26hZjm9Cc4NMFsbBrDDDsR4_J23DPPmieDGQs8X-tp8-3Txdfzz-31zeXV-cfr1rEezy0fvMK-J4PgsqdKCNVZqZT31DtBDCGYOTN4rIw1htgBjGKWYSGp8JZj3p027UG3_IbNYvUmh8nkrU4m6HX0s3aguSJEdZV_feA3Of1aoMx6CsXBOJoI9cuayJ6JrpcV5Aew2lJKhuGfNMF6F4Pex6B3HmtM9T4Gzerey_XAYifwD1ur7xV4tQKmODMO2UQXygPHWF_P95U7O3BQ7bsLkHVxAaIDHzK4WfsU_vOUewKBpXg</recordid><startdate>20030205</startdate><enddate>20030205</enddate><creator>Paulsson, Birgit</creator><creator>Kotova, Natalia</creator><creator>Grawé, Jan</creator><creator>Henderson, Alistair</creator><creator>Granath, Fredrik</creator><creator>Golding, Bernard</creator><creator>Törnqvist, Margareta</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>7U7</scope><scope>C1K</scope><scope>ADTPV</scope><scope>AOWAS</scope></search><sort><creationdate>20030205</creationdate><title>Induction of micronuclei in mouse and rat by glycidamide, genotoxic metabolite of acrylamide</title><author>Paulsson, Birgit ; Kotova, Natalia ; Grawé, Jan ; Henderson, Alistair ; Granath, Fredrik ; Golding, Bernard ; Törnqvist, Margareta</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c460t-5fd90d61f7586297793b899dd2dc71a1104cafd09abaa1bfea94b407827db5053</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2003</creationdate><topic>Acrylamide</topic><topic>Acrylamide - administration & dosage</topic><topic>Acrylamide - metabolism</topic><topic>Acrylamide - toxicity</topic><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Carcinogenic</topic><topic>Chemical mutagenesis</topic><topic>Dose-Response Relationship, Drug</topic><topic>Epoxy Compounds - administration & dosage</topic><topic>Epoxy Compounds - metabolism</topic><topic>Epoxy Compounds - toxicity</topic><topic>Erythrocytes - drug effects</topic><topic>Erythrocytes - metabolism</topic><topic>Erythrocytes - ultrastructure</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Glycidamide</topic><topic>Hemoglobin adducts</topic><topic>Hemoglobins - chemistry</topic><topic>Hemoglobins - drug effects</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Mice</topic><topic>Mice, Inbred CBA</topic><topic>Micronuclei</topic><topic>Micronuclei, Chromosome-Defective - drug effects</topic><topic>Micronucleus Tests</topic><topic>Molecular and cellular biology</topic><topic>Molecular genetics</topic><topic>Mutagenesis. Repair</topic><topic>Mutagens - administration & dosage</topic><topic>Mutagens - toxicity</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Toxicology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Paulsson, Birgit</creatorcontrib><creatorcontrib>Kotova, Natalia</creatorcontrib><creatorcontrib>Grawé, Jan</creatorcontrib><creatorcontrib>Henderson, Alistair</creatorcontrib><creatorcontrib>Granath, Fredrik</creatorcontrib><creatorcontrib>Golding, Bernard</creatorcontrib><creatorcontrib>Törnqvist, Margareta</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>Toxicology Abstracts</collection><collection>Environmental Sciences and Pollution Management</collection><collection>SwePub</collection><collection>SwePub Articles</collection><jtitle>Mutation research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Paulsson, Birgit</au><au>Kotova, Natalia</au><au>Grawé, Jan</au><au>Henderson, Alistair</au><au>Granath, Fredrik</au><au>Golding, Bernard</au><au>Törnqvist, Margareta</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Induction of micronuclei in mouse and rat by glycidamide, genotoxic metabolite of acrylamide</atitle><jtitle>Mutation research</jtitle><addtitle>Mutat Res</addtitle><date>2003-02-05</date><risdate>2003</risdate><volume>535</volume><issue>1</issue><spage>15</spage><epage>24</epage><pages>15-24</pages><issn>1383-5718</issn><issn>0027-5107</issn><eissn>1879-3592</eissn><abstract>Male CBA mice and male Sprague–Dawley rats were treated by i.p. injection of glycidamide (GA), the presumed genotoxic metabolite of acrylamide (AA). GA was obtained through a new way of synthesis. As an endpoint of chromosome damage, micronucleus (MN) induction in erythrocytes was measured. Hemoglobin (Hb) adducts were used as a measure of in vivo dose of GA. GA induced linear dose-dependent increases in adduct levels in both species. Rats exhibit, compared with mice, 30% higher Hb adduct levels per unit of administered amount of GA. The incremental MN frequencies per administered dose of GA in mice showed a linear-quadratic dose-dependent curve. In the rat no positive dose–response relationship was obtained, probably due to toxic effects to the bone marrow. The main result of this study is the finding that after treatment with synthetic GA the MN frequency per unit of the in vivo dose of GA in the mouse is very similar to that obtained in a previous study, where animals were treated with AA and GA as a metabolite. This equality in potency of GA, whether its in vivo dose is established by injection of synthetic GA or through metabolism of AA, supports the view that GA is the predominant genotoxic factor in AA exposure.</abstract><cop>Amsterdam</cop><pub>Elsevier B.V</pub><pmid>12547279</pmid><doi>10.1016/S1383-5718(02)00281-4</doi><tpages>10</tpages></addata></record> |
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| ispartof | Mutation research, 2003-02, Vol.535 (1), p.15-24 |
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| subjects | Acrylamide Acrylamide - administration & dosage Acrylamide - metabolism Acrylamide - toxicity Animals Biological and medical sciences Carcinogenic Chemical mutagenesis Dose-Response Relationship, Drug Epoxy Compounds - administration & dosage Epoxy Compounds - metabolism Epoxy Compounds - toxicity Erythrocytes - drug effects Erythrocytes - metabolism Erythrocytes - ultrastructure Fundamental and applied biological sciences. Psychology Glycidamide Hemoglobin adducts Hemoglobins - chemistry Hemoglobins - drug effects Male Medical sciences Mice Mice, Inbred CBA Micronuclei Micronuclei, Chromosome-Defective - drug effects Micronucleus Tests Molecular and cellular biology Molecular genetics Mutagenesis. Repair Mutagens - administration & dosage Mutagens - toxicity Rats Rats, Sprague-Dawley Toxicology |
| title | Induction of micronuclei in mouse and rat by glycidamide, genotoxic metabolite of acrylamide |
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