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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<front><div type="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.</div>
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Department of Chemical Toxicology, Division of Environmental Medicine, Norwegian Institute of Public Health, Nydalen, NO-0403 Oslo, Norway</aff>
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Norwegian Radiation Protection Authority, NO-1332 Østerås, Norway</aff>
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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>
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<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>
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<name type="personal"><namePart type="given">Ann-Karin</namePart>
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<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>
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</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>
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</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>
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<subject><topic>IN VITRO METHODS AND ALTERNATIVES TO ANIMALS</topic>
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<dateIssued encoding="w3cdtf">2010-01-13</dateIssued>
<dateCreated encoding="w3cdtf">2010-01-13</dateCreated>
<copyrightDate encoding="w3cdtf">2010</copyrightDate>
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<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>
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<topic>octyl methoxycinnamate</topic>
<topic>cyclobutane pyrimidine dimers</topic>
<topic>oxidative DNA lesions</topic>
<topic>UV</topic>
<topic>sunscreens</topic>
<topic>gene expression</topic>
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<relatedItem type="host"><titleInfo><title>Toxicological Sciences</title>
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<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>
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<detail type="issue"><caption>no.</caption>
<number>2</number>
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<extent unit="pages"><start>272</start>
<end>284</end>
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<identifier type="DOI">10.1093/toxsci/kfq005</identifier>
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