Octyl Methoxycinnamate Modulates Gene Expression and Prevents Cyclobutane Pyrimidine Dimer Formation but not Oxidative DNA Damage in UV-Exposed Human Cell Lines
Identifieur interne : 001875 ( Istex/Corpus ); précédent : 001874; suivant : 001876Octyl Methoxycinnamate Modulates Gene Expression and Prevents Cyclobutane Pyrimidine Dimer Formation but not Oxidative DNA Damage in UV-Exposed Human Cell Lines
Auteurs : Nur Duale ; Ann-Karin Olsen ; Terje Christensen ; Shamas T. Butt ; Gunnar BrunborgSource :
- Toxicological Sciences [ 1096-6080 ] ; 2010-01-13.
Abstract
Octyl methoxycinnamate (OMC) is one of the most widely used sunscreen ingredients. To analyze biological effects of OMC, an in vitro approach was used implying ultraviolet (UV) exposure of two human cell lines, a primary skin fibroblast (GM00498) and a breast cancer (MCF-7) cell lines. End points include cell viability assessment, assay of cyclobutane pyrimidine dimers (CPDs) and oxidated DNA lesions using alkaline elution and lesion-specific enzymes, and gene expression analysis of a panel of 17 DNA damageresponsive genes. We observed that OMC provided protection against CPDs, and the degree of protection correlated with the OMC-mediated reduction in UV dose. No such protection was found with respect to oxidative DNA lesions. Upon UV exposure in the presence of OMC, the gene expression studies showed significant differential changes in some of the genes studied and the expression of p53 protein was also changed. For some genes, the change in expression seemed to be delayed in time by OMC. The experimental approach applied in this study, using a panel of 17 genes in an in vitro cellular system together with genotoxicity assays, may be useful in the initial screening of active ingredients in sunscreens.
Url:
DOI: 10.1093/toxsci/kfq005
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ISTEX:E52432439993D93C5C196F00C2FEA28F4E9DF853Le document en format XML
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To analyze biological effects of OMC, an in vitro approach was used implying ultraviolet (UV) exposure of two human cell lines, a primary skin fibroblast (GM00498) and a breast cancer (MCF-7) cell lines. End points include cell viability assessment, assay of cyclobutane pyrimidine dimers (CPDs) and oxidated DNA lesions using alkaline elution and lesion-specific enzymes, and gene expression analysis of a panel of 17 DNA damageresponsive genes. We observed that OMC provided protection against CPDs, and the degree of protection correlated with the OMC-mediated reduction in UV dose. No such protection was found with respect to oxidative DNA lesions. Upon UV exposure in the presence of OMC, the gene expression studies showed significant differential changes in some of the genes studied and the expression of p53 protein was also changed. For some genes, the change in expression seemed to be delayed in time by OMC. The experimental approach applied in this study, using a panel of 17 genes in an in vitro cellular system together with genotoxicity assays, may be useful in the initial screening of active ingredients in sunscreens.</div></front></TEI><istex><corpusName>oup</corpusName><author><json:item><name>Nur Duale</name><affiliations><json:string>Department of Chemical Toxicology, Division of Environmental Medicine, Norwegian Institute of Public Health, Nydalen, NO-0403 Oslo, Norway</json:string></affiliations></json:item><json:item><name>Ann-Karin Olsen</name><affiliations><json:string>Department of Chemical Toxicology, Division of Environmental Medicine, Norwegian Institute of Public Health, Nydalen, NO-0403 Oslo, Norway</json:string></affiliations></json:item><json:item><name>Terje Christensen</name><affiliations><json:string>Norwegian Radiation Protection Authority, NO-1332 sters, Norway</json:string></affiliations></json:item><json:item><name>Shamas T. 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To analyze biological effects of OMC, an in vitro approach was used implying ultraviolet (UV) exposure of two human cell lines, a primary skin fibroblast (GM00498) and a breast cancer (MCF-7) cell lines. End points include cell viability assessment, assay of cyclobutane pyrimidine dimers (CPDs) and oxidated DNA lesions using alkaline elution and lesion-specific enzymes, and gene expression analysis of a panel of 17 DNA damageresponsive genes. We observed that OMC provided protection against CPDs, and the degree of protection correlated with the OMC-mediated reduction in UV dose. No such protection was found with respect to oxidative DNA lesions. Upon UV exposure in the presence of OMC, the gene expression studies showed significant differential changes in some of the genes studied and the expression of p53 protein was also changed. For some genes, the change in expression seemed to be delayed in time by OMC. The experimental approach applied in this study, using a panel of 17 genes in an in vitro cellular system together with genotoxicity assays, may be useful in the initial screening of active ingredients in sunscreens.</p></abstract><textClass><keywords scheme="keyword"><list><item><term>IN VITRO METHODS AND ALTERNATIVES TO ANIMALS</term></item></list></keywords></textClass><textClass><keywords scheme="keyword"><list><head>keywords</head><item><term>octyl methoxycinnamate</term></item><item><term>cyclobutane pyrimidine dimers</term></item><item><term>oxidative DNA lesions</term></item><item><term>UV</term></item><item><term>sunscreens</term></item><item><term>gene expression</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="2010-01-13">Created</change><change when="2010-01-13">Published</change><change xml:id="refBibs-istex" who="#ISTEX-API" when="2016-10-14">References added</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/E52432439993D93C5C196F00C2FEA28F4E9DF853/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="corpus oup" wicri:toSee="no header"><istex:docType PUBLIC="-//NLM//DTD Journal Publishing DTD v2.3 20070202//EN" URI="journalpublishing.dtd" name="istex:docType"></istex:docType><istex:document><article article-type="research-article"><front><journal-meta><journal-id journal-id-type="hwp">toxsci</journal-id><journal-id journal-id-type="publisher-id">toxsci</journal-id><journal-title>Toxicological Sciences</journal-title><issn pub-type="epub">1096-0929</issn><issn pub-type="ppub">1096-6080</issn><publisher><publisher-name>Oxford University Press</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="doi">10.1093/toxsci/kfq005</article-id><article-categories><subj-group><subject><italic>IN VITRO</italic> METHODS AND ALTERNATIVES TO ANIMALS</subject></subj-group></article-categories><title-group><article-title>Octyl Methoxycinnamate Modulates Gene Expression and Prevents Cyclobutane Pyrimidine Dimer Formation but not Oxidative DNA Damage in UV-Exposed Human Cell Lines</article-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Duale</surname><given-names>Nur</given-names></name><xref ref-type="aff" rid="aff1">*</xref></contrib><contrib contrib-type="author"><name><surname>Olsen</surname><given-names>Ann-Karin</given-names></name><xref ref-type="aff" rid="aff1">*</xref></contrib><contrib contrib-type="author"><name><surname>Christensen</surname><given-names>Terje</given-names></name><xref ref-type="aff" rid="aff2">†</xref></contrib><contrib contrib-type="author"><name><surname>Butt</surname><given-names>Shamas T.</given-names></name><xref ref-type="aff" rid="aff2">†</xref></contrib><contrib contrib-type="author" corresp="yes"><name><surname>Brunborg</surname><given-names>Gunnar</given-names></name><xref ref-type="aff" rid="aff1">*</xref><xref ref-type="corresp" rid="cor1">1</xref></contrib></contrib-group><aff id="aff1"><label>*</label>Department of Chemical Toxicology, Division of Environmental Medicine, Norwegian Institute of Public Health, Nydalen, NO-0403 Oslo, Norway</aff><aff id="aff2"><label>†</label>Norwegian Radiation Protection Authority, NO-1332 Østerås, Norway</aff><author-notes><corresp id="cor1"><label>1</label>To whom correspondence should be addressed at Department of Chemical Toxicology, Division of Environmental Medicine, Norwegian Institute of Public Health, PO Box 4404, Nydalen, NO-0403 Oslo, Norway. Fax: +47-2107-6686. E-mail: <email>gunnar.brunborg@fhi.no</email>.</corresp></author-notes><pub-date pub-type="epub-ppub"><month>4</month><year>2010</year></pub-date><pub-date pub-type="epub"><day>13</day><month>1</month><year>2010</year></pub-date><volume>114</volume><issue>2</issue><fpage>272</fpage><lpage>284</lpage><history><date date-type="received"><day>15</day><month>10</month><year>2009</year></date><date date-type="accepted"><day>18</day><month>12</month><year>2009</year></date></history><permissions><copyright-statement>© The Author 2010. Published by Oxford University Press on behalf of the Society of Toxicology. For permissions, please email: journals.permissions@oxfordjournals.org.</copyright-statement><copyright-year>2010</copyright-year><license license-type="open-access"><p>This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/2.5), which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.</p></license></permissions><abstract><p>Octyl methoxycinnamate (OMC) is one of the most widely used sunscreen ingredients. To analyze biological effects of OMC, an <italic>in vitro</italic> approach was used implying ultraviolet (UV) exposure of two human cell lines, a primary skin fibroblast (GM00498) and a breast cancer (MCF-7) cell lines. End points include cell viability assessment, assay of cyclobutane pyrimidine dimers (CPDs) and oxidated DNA lesions using alkaline elution and lesion-specific enzymes, and gene expression analysis of a panel of 17 DNA damage–responsive genes. We observed that OMC provided protection against CPDs, and the degree of protection correlated with the OMC-mediated reduction in UV dose. No such protection was found with respect to oxidative DNA lesions. Upon UV exposure in the presence of OMC, the gene expression studies showed significant differential changes in some of the genes studied and the expression of p53 protein was also changed. For some genes, the change in expression seemed to be delayed in time by OMC. The experimental approach applied in this study, using a panel of 17 genes in an <italic>in vitro</italic> cellular system together with genotoxicity assays, may be useful in the initial screening of active ingredients in sunscreens.</p></abstract><kwd-group><kwd>octyl methoxycinnamate</kwd><kwd>cyclobutane pyrimidine dimers</kwd><kwd>oxidative DNA lesions</kwd><kwd>UV</kwd><kwd>sunscreens</kwd><kwd>gene expression</kwd></kwd-group></article-meta></front></article></istex:document></istex:metadataXml><mods version="3.6"><titleInfo><title>Octyl Methoxycinnamate Modulates Gene Expression and Prevents Cyclobutane Pyrimidine Dimer Formation but not Oxidative DNA Damage in UV-Exposed Human Cell Lines</title></titleInfo><titleInfo type="alternative" contentType="CDATA"><title>Octyl Methoxycinnamate Modulates Gene Expression and Prevents Cyclobutane Pyrimidine Dimer Formation but not Oxidative DNA Damage in UV-Exposed Human Cell Lines</title></titleInfo><name type="personal"><namePart type="given">Nur</namePart><namePart type="family">Duale</namePart><affiliation>Department of Chemical Toxicology, Division of Environmental Medicine, Norwegian Institute of Public Health, Nydalen, NO-0403 Oslo, Norway</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Ann-Karin</namePart><namePart type="family">Olsen</namePart><affiliation>Department of Chemical Toxicology, Division of Environmental Medicine, Norwegian Institute of Public Health, Nydalen, NO-0403 Oslo, Norway</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Terje</namePart><namePart type="family">Christensen</namePart><affiliation>Norwegian Radiation Protection Authority, NO-1332 sters, Norway</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Shamas T.</namePart><namePart type="family">Butt</namePart><affiliation>Norwegian Radiation Protection Authority, NO-1332 sters, Norway</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal" displayLabel="corresp"><namePart type="given">Gunnar</namePart><namePart type="family">Brunborg</namePart><affiliation>Department of Chemical Toxicology, Division of Environmental Medicine, Norwegian Institute of Public Health, Nydalen, NO-0403 Oslo, Norway</affiliation><affiliation>E-mail: gunnar.brunborg@fhi.no</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="research-article" displayLabel="research-article"></genre><subject><topic>IN VITRO METHODS AND ALTERNATIVES TO ANIMALS</topic></subject><originInfo><publisher>Oxford University Press</publisher><dateIssued encoding="w3cdtf">2010-01-13</dateIssued><dateCreated encoding="w3cdtf">2010-01-13</dateCreated><copyrightDate encoding="w3cdtf">2010</copyrightDate></originInfo><language><languageTerm type="code" authority="iso639-2b">eng</languageTerm><languageTerm type="code" authority="rfc3066">en</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType></physicalDescription><abstract>Octyl methoxycinnamate (OMC) is one of the most widely used sunscreen ingredients. To analyze biological effects of OMC, an in vitro approach was used implying ultraviolet (UV) exposure of two human cell lines, a primary skin fibroblast (GM00498) and a breast cancer (MCF-7) cell lines. End points include cell viability assessment, assay of cyclobutane pyrimidine dimers (CPDs) and oxidated DNA lesions using alkaline elution and lesion-specific enzymes, and gene expression analysis of a panel of 17 DNA damageresponsive genes. We observed that OMC provided protection against CPDs, and the degree of protection correlated with the OMC-mediated reduction in UV dose. No such protection was found with respect to oxidative DNA lesions. Upon UV exposure in the presence of OMC, the gene expression studies showed significant differential changes in some of the genes studied and the expression of p53 protein was also changed. For some genes, the change in expression seemed to be delayed in time by OMC. The experimental approach applied in this study, using a panel of 17 genes in an in vitro cellular system together with genotoxicity assays, may be useful in the initial screening of active ingredients in sunscreens.</abstract><subject><genre>keywords</genre><topic>octyl methoxycinnamate</topic><topic>cyclobutane pyrimidine dimers</topic><topic>oxidative DNA lesions</topic><topic>UV</topic><topic>sunscreens</topic><topic>gene expression</topic></subject><relatedItem type="host"><titleInfo><title>Toxicological Sciences</title></titleInfo><genre type="journal">journal</genre><identifier type="ISSN">1096-6080</identifier><identifier type="eISSN">1096-0929</identifier><identifier type="PublisherID">toxsci</identifier><identifier type="PublisherID-hwp">toxsci</identifier><part><date>2010</date><detail type="volume"><caption>vol.</caption><number>114</number></detail><detail type="issue"><caption>no.</caption><number>2</number></detail><extent unit="pages"><start>272</start><end>284</end></extent></part></relatedItem><identifier type="istex">E52432439993D93C5C196F00C2FEA28F4E9DF853</identifier><identifier type="DOI">10.1093/toxsci/kfq005</identifier><accessCondition type="use and reproduction" contentType="open-access">This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/2.5), which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.</accessCondition><recordInfo><recordContentSource>OUP</recordContentSource></recordInfo></mods></metadata><covers><json:item><original>true</original><mimetype>image/tiff</mimetype><extension>tiff</extension><uri>https://api.istex.fr/document/E52432439993D93C5C196F00C2FEA28F4E9DF853/covers/tiff</uri></json:item><json:item><original>true</original><mimetype>text/html</mimetype><extension>html</extension><uri>https://api.istex.fr/document/E52432439993D93C5C196F00C2FEA28F4E9DF853/covers/html</uri></json:item></covers><annexes><json:item><original>true</original><mimetype>image/jpeg</mimetype><extension>jpeg</extension><uri>https://api.istex.fr/document/E52432439993D93C5C196F00C2FEA28F4E9DF853/annexes/jpeg</uri></json:item><json:item><original>true</original><mimetype>image/gif</mimetype><extension>gif</extension><uri>https://api.istex.fr/document/E52432439993D93C5C196F00C2FEA28F4E9DF853/annexes/gif</uri></json:item><json:item><original>true</original><mimetype>application/pdf</mimetype><extension>pdf</extension><uri>https://api.istex.fr/document/E52432439993D93C5C196F00C2FEA28F4E9DF853/annexes/pdf</uri></json:item></annexes><enrichments><istex:catWosTEI uri="https://api.istex.fr/document/E52432439993D93C5C196F00C2FEA28F4E9DF853/enrichments/catWos"><teiHeader><profileDesc><textClass><classCode scheme="WOS">TOXICOLOGY</classCode><classCode scheme="WOS">TRANSPLANTATION</classCode></textClass></profileDesc></teiHeader></istex:catWosTEI><json:item><type>refBibs</type><uri>https://api.istex.fr/document/E52432439993D93C5C196F00C2FEA28F4E9DF853/enrichments/refBibs</uri></json:item></enrichments><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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