Activation of aryl hydrocarbon receptor signaling by extracts of teak and other wood dusts.
Identifieur interne : 001F04 ( Main/Exploration ); précédent : 001F03; suivant : 001F05Activation of aryl hydrocarbon receptor signaling by extracts of teak and other wood dusts.
Auteurs : Mark J. Wilson ; Gabriele Sabbioni ; Roy Rando ; Charles A. MillerSource :
- Environmental toxicology [ 1522-7278 ] ; 2015.
Descripteurs français
- KwdFr :
- Animaux (MeSH), Anthraquinones (composition chimique), Anthraquinones (toxicité), Bois (composition chimique), Cellules HepG2 (MeSH), Cytochrome P-450 CYP1A1 (génétique), Cytochrome P-450 CYP1A1 (métabolisme), Humains (MeSH), Méthanol (composition chimique), Poussière (analyse), Récepteurs à hydrocarbure aromatique (métabolisme), Régulation de l'expression des gènes (MeSH), Transduction du signal (effets des médicaments et des substances chimiques).
- MESH :
- analyse : Poussière.
- composition chimique : Anthraquinones, Bois, Méthanol.
- effets des médicaments et des substances chimiques : Transduction du signal.
- génétique : Cytochrome P-450 CYP1A1.
- métabolisme : Cytochrome P-450 CYP1A1, Récepteurs à hydrocarbure aromatique.
- toxicité : Anthraquinones.
- Animaux, Cellules HepG2, Humains, Régulation de l'expression des gènes.
English descriptors
- KwdEn :
- Animals (MeSH), Anthraquinones (chemistry), Anthraquinones (toxicity), Cytochrome P-450 CYP1A1 (genetics), Cytochrome P-450 CYP1A1 (metabolism), Dust (analysis), Gene Expression Regulation (MeSH), Hep G2 Cells (MeSH), Humans (MeSH), Methanol (chemistry), Receptors, Aryl Hydrocarbon (metabolism), Signal Transduction (drug effects), Wood (chemistry).
- MESH :
- chemical , analysis : Dust.
- chemical , chemistry : Anthraquinones, Methanol.
- chemical , genetics : Cytochrome P-450 CYP1A1.
- chemical , metabolism : Cytochrome P-450 CYP1A1, Receptors, Aryl Hydrocarbon.
- chemical , toxicity : Anthraquinones.
- chemistry : Wood.
- drug effects : Signal Transduction.
- Animals, Gene Expression Regulation, Hep G2 Cells, Humans.
Abstract
Wood dusts, as a group, are categorized as known human carcinogens, but the risks of exposure to specific types of wood dusts and the carcinogenic chemicals they contain are not well studied. Aryl hydrocarbon receptor (AhR) is a ligand-activated transcription factor that is linked to the carcinogenic action of specific classes of chemicals. Here we examined whether chemicals in various wood dusts had the potential to activate AhR signaling as a potential toxic mechanism of action. We found that methanol extracts of teak, walnut, mahogany, and poplar dusts contained a wide range of AhR ligand activity, whereas extracts of oak, pine, and other softwoods did not contain appreciable activity. Teak dust extract, being particularly potent, was subjected to chemical analysis. The 2-methylanthraquinone (2-MAQ) accounted for the AhR ligand activity and was present at an average concentration of 0.27 parts per hundred in teak dust. Pure 2-MAQ potently induced AhR signaling (EC50 115 nM), confirming that this was the active ligand. Aqueous extracts of teak dust made using yeast or mammalian cell culture medium also contained robust AhR activity, suggesting the 2-MAQ ligand is soluble at bioactive concentrations in physiologically relevant fluids. The high concentration and potency of 2-MAQ in teak wood suggest it may mediate toxic effects through activation of AhR signaling in exposed wood workers.
DOI: 10.1002/tox.22007
PubMed: 24898320
Affiliations:
Links toward previous steps (curation, corpus...)
Le document en format XML
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Wilson</name><affiliation><nlm:affiliation>Department of Global Environmental Health Sciences, Tulane University School of Public Health and Tropical Medicine, New Orleans, Louisiana, 70112.</nlm:affiliation><wicri:noCountry code="subField">70112</wicri:noCountry></affiliation></author><author><name sortKey="Sabbioni, Gabriele" sort="Sabbioni, Gabriele" uniqKey="Sabbioni G" first="Gabriele" last="Sabbioni">Gabriele Sabbioni</name><affiliation><nlm:affiliation>Department of Global Environmental Health Sciences, Tulane University School of Public Health and Tropical Medicine, New Orleans, Louisiana, 70112.</nlm:affiliation><wicri:noCountry code="subField">70112</wicri:noCountry></affiliation></author><author><name sortKey="Rando, Roy" sort="Rando, Roy" uniqKey="Rando R" first="Roy" last="Rando">Roy Rando</name><affiliation><nlm:affiliation>Department of Global Environmental Health Sciences, Tulane University School of Public Health and Tropical Medicine, New Orleans, Louisiana, 70112.</nlm:affiliation><wicri:noCountry code="subField">70112</wicri:noCountry></affiliation></author><author><name sortKey="Miller, Charles A" sort="Miller, Charles A" uniqKey="Miller C" first="Charles A" last="Miller">Charles A. 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Wilson</name><affiliation><nlm:affiliation>Department of Global Environmental Health Sciences, Tulane University School of Public Health and Tropical Medicine, New Orleans, Louisiana, 70112.</nlm:affiliation><wicri:noCountry code="subField">70112</wicri:noCountry></affiliation></author><author><name sortKey="Sabbioni, Gabriele" sort="Sabbioni, Gabriele" uniqKey="Sabbioni G" first="Gabriele" last="Sabbioni">Gabriele Sabbioni</name><affiliation><nlm:affiliation>Department of Global Environmental Health Sciences, Tulane University School of Public Health and Tropical Medicine, New Orleans, Louisiana, 70112.</nlm:affiliation><wicri:noCountry code="subField">70112</wicri:noCountry></affiliation></author><author><name sortKey="Rando, Roy" sort="Rando, Roy" uniqKey="Rando R" first="Roy" last="Rando">Roy Rando</name><affiliation><nlm:affiliation>Department of Global Environmental Health Sciences, Tulane University School of Public Health and Tropical Medicine, New Orleans, Louisiana, 70112.</nlm:affiliation><wicri:noCountry code="subField">70112</wicri:noCountry></affiliation></author><author><name sortKey="Miller, Charles A" sort="Miller, Charles A" uniqKey="Miller C" first="Charles A" last="Miller">Charles A. Miller</name><affiliation><nlm:affiliation>Department of Global Environmental Health Sciences, Tulane University School of Public Health and Tropical Medicine, New Orleans, Louisiana, 70112.</nlm:affiliation><wicri:noCountry code="subField">70112</wicri:noCountry></affiliation></author></analytic><series><title level="j">Environmental toxicology</title><idno type="eISSN">1522-7278</idno><imprint><date when="2015" type="published">2015</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals (MeSH)</term><term>Anthraquinones (chemistry)</term><term>Anthraquinones (toxicity)</term><term>Cytochrome P-450 CYP1A1 (genetics)</term><term>Cytochrome P-450 CYP1A1 (metabolism)</term><term>Dust (analysis)</term><term>Gene Expression Regulation (MeSH)</term><term>Hep G2 Cells (MeSH)</term><term>Humans (MeSH)</term><term>Methanol (chemistry)</term><term>Receptors, Aryl Hydrocarbon (metabolism)</term><term>Signal Transduction (drug effects)</term><term>Wood (chemistry)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Animaux (MeSH)</term><term>Anthraquinones (composition chimique)</term><term>Anthraquinones (toxicité)</term><term>Bois (composition chimique)</term><term>Cellules HepG2 (MeSH)</term><term>Cytochrome P-450 CYP1A1 (génétique)</term><term>Cytochrome P-450 CYP1A1 (métabolisme)</term><term>Humains (MeSH)</term><term>Méthanol (composition chimique)</term><term>Poussière (analyse)</term><term>Récepteurs à hydrocarbure aromatique (métabolisme)</term><term>Régulation de l'expression des gènes (MeSH)</term><term>Transduction du signal (effets des médicaments et des substances chimiques)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="analysis" xml:lang="en"><term>Dust</term></keywords><keywords scheme="MESH" type="chemical" qualifier="chemistry" xml:lang="en"><term>Anthraquinones</term><term>Methanol</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Cytochrome P-450 CYP1A1</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Cytochrome P-450 CYP1A1</term><term>Receptors, Aryl Hydrocarbon</term></keywords><keywords scheme="MESH" type="chemical" qualifier="toxicity" xml:lang="en"><term>Anthraquinones</term></keywords><keywords scheme="MESH" qualifier="analyse" xml:lang="fr"><term>Poussière</term></keywords><keywords scheme="MESH" qualifier="chemistry" xml:lang="en"><term>Wood</term></keywords><keywords scheme="MESH" qualifier="composition chimique" xml:lang="fr"><term>Anthraquinones</term><term>Bois</term><term>Méthanol</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Signal Transduction</term></keywords><keywords scheme="MESH" qualifier="effets des médicaments et des substances chimiques" xml:lang="fr"><term>Transduction du signal</term></keywords><keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Cytochrome P-450 CYP1A1</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Cytochrome P-450 CYP1A1</term><term>Récepteurs à hydrocarbure aromatique</term></keywords><keywords scheme="MESH" qualifier="toxicité" xml:lang="fr"><term>Anthraquinones</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Gene Expression Regulation</term><term>Hep G2 Cells</term><term>Humans</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Cellules HepG2</term><term>Humains</term><term>Régulation de l'expression des gènes</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Wood dusts, as a group, are categorized as known human carcinogens, but the risks of exposure to specific types of wood dusts and the carcinogenic chemicals they contain are not well studied. Aryl hydrocarbon receptor (AhR) is a ligand-activated transcription factor that is linked to the carcinogenic action of specific classes of chemicals. Here we examined whether chemicals in various wood dusts had the potential to activate AhR signaling as a potential toxic mechanism of action. We found that methanol extracts of teak, walnut, mahogany, and poplar dusts contained a wide range of AhR ligand activity, whereas extracts of oak, pine, and other softwoods did not contain appreciable activity. Teak dust extract, being particularly potent, was subjected to chemical analysis. The 2-methylanthraquinone (2-MAQ) accounted for the AhR ligand activity and was present at an average concentration of 0.27 parts per hundred in teak dust. Pure 2-MAQ potently induced AhR signaling (EC50 115 nM), confirming that this was the active ligand. Aqueous extracts of teak dust made using yeast or mammalian cell culture medium also contained robust AhR activity, suggesting the 2-MAQ ligand is soluble at bioactive concentrations in physiologically relevant fluids. The high concentration and potency of 2-MAQ in teak wood suggest it may mediate toxic effects through activation of AhR signaling in exposed wood workers.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" IndexingMethod="Curated" Owner="NLM"><PMID Version="1">24898320</PMID><DateCompleted><Year>2016</Year><Month>06</Month><Day>10</Day></DateCompleted><DateRevised><Year>2018</Year><Month>12</Month><Day>02</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1522-7278</ISSN><JournalIssue CitedMedium="Internet"><Volume>30</Volume><Issue>12</Issue><PubDate><Year>2015</Year><Month>Dec</Month></PubDate></JournalIssue><Title>Environmental toxicology</Title><ISOAbbreviation>Environ Toxicol</ISOAbbreviation></Journal><ArticleTitle>Activation of aryl hydrocarbon receptor signaling by extracts of teak and other wood dusts.</ArticleTitle><Pagination><MedlinePgn>1375-84</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1002/tox.22007</ELocationID><Abstract><AbstractText>Wood dusts, as a group, are categorized as known human carcinogens, but the risks of exposure to specific types of wood dusts and the carcinogenic chemicals they contain are not well studied. Aryl hydrocarbon receptor (AhR) is a ligand-activated transcription factor that is linked to the carcinogenic action of specific classes of chemicals. Here we examined whether chemicals in various wood dusts had the potential to activate AhR signaling as a potential toxic mechanism of action. We found that methanol extracts of teak, walnut, mahogany, and poplar dusts contained a wide range of AhR ligand activity, whereas extracts of oak, pine, and other softwoods did not contain appreciable activity. Teak dust extract, being particularly potent, was subjected to chemical analysis. The 2-methylanthraquinone (2-MAQ) accounted for the AhR ligand activity and was present at an average concentration of 0.27 parts per hundred in teak dust. Pure 2-MAQ potently induced AhR signaling (EC50 115 nM), confirming that this was the active ligand. Aqueous extracts of teak dust made using yeast or mammalian cell culture medium also contained robust AhR activity, suggesting the 2-MAQ ligand is soluble at bioactive concentrations in physiologically relevant fluids. The high concentration and potency of 2-MAQ in teak wood suggest it may mediate toxic effects through activation of AhR signaling in exposed wood workers.</AbstractText><CopyrightInformation>© 2014 Wiley Periodicals, Inc.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Wilson</LastName><ForeName>Mark J</ForeName><Initials>MJ</Initials><AffiliationInfo><Affiliation>Department of Global Environmental Health Sciences, Tulane University School of Public Health and Tropical Medicine, New Orleans, Louisiana, 70112.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Sabbioni</LastName><ForeName>Gabriele</ForeName><Initials>G</Initials><AffiliationInfo><Affiliation>Department of Global Environmental Health Sciences, Tulane University School of Public Health and Tropical Medicine, New Orleans, Louisiana, 70112.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Rando</LastName><ForeName>Roy</ForeName><Initials>R</Initials><AffiliationInfo><Affiliation>Department of Global Environmental Health Sciences, Tulane University School of Public Health and Tropical Medicine, New Orleans, Louisiana, 70112.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Miller</LastName><ForeName>Charles A</ForeName><Initials>CA</Initials><Suffix>3rd</Suffix><AffiliationInfo><Affiliation>Department of Global Environmental Health Sciences, Tulane University School of Public Health and Tropical Medicine, New Orleans, Louisiana, 70112.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2014</Year><Month>06</Month><Day>05</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Environ Toxicol</MedlineTA><NlmUniqueID>100885357</NlmUniqueID><ISSNLinking>1520-4081</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000880">Anthraquinones</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D004391">Dust</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D018336">Receptors, Aryl Hydrocarbon</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 1.14.14.1</RegistryNumber><NameOfSubstance UI="D019363">Cytochrome P-450 CYP1A1</NameOfSubstance></Chemical><Chemical><RegistryNumber>Q9P233HWAJ</RegistryNumber><NameOfSubstance UI="C073955">2-methylanthraquinone</NameOfSubstance></Chemical><Chemical><RegistryNumber>Y4S76JWI15</RegistryNumber><NameOfSubstance UI="D000432">Methanol</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000880" MajorTopicYN="N">Anthraquinones</DescriptorName><QualifierName UI="Q000737" MajorTopicYN="N">chemistry</QualifierName><QualifierName UI="Q000633" MajorTopicYN="N">toxicity</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D019363" MajorTopicYN="N">Cytochrome P-450 CYP1A1</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D004391" MajorTopicYN="N">Dust</DescriptorName><QualifierName UI="Q000032" MajorTopicYN="Y">analysis</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005786" MajorTopicYN="N">Gene Expression Regulation</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D056945" MajorTopicYN="N">Hep G2 Cells</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000432" MajorTopicYN="N">Methanol</DescriptorName><QualifierName UI="Q000737" MajorTopicYN="N">chemistry</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D018336" MajorTopicYN="N">Receptors, Aryl Hydrocarbon</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015398" MajorTopicYN="N">Signal Transduction</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D014934" MajorTopicYN="N">Wood</DescriptorName><QualifierName UI="Q000737" MajorTopicYN="Y">chemistry</QualifierName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">2-methylanthraquinone</Keyword><Keyword MajorTopicYN="N">aryl hydrocarbon receptor</Keyword><Keyword MajorTopicYN="N">sinonasal cancer</Keyword><Keyword MajorTopicYN="N">teak</Keyword><Keyword MajorTopicYN="N">wood dust</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2014</Year><Month>04</Month><Day>18</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2014</Year><Month>05</Month><Day>19</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2014</Year><Month>05</Month><Day>27</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2014</Year><Month>6</Month><Day>6</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2014</Year><Month>6</Month><Day>6</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2016</Year><Month>6</Month><Day>11</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">24898320</ArticleId><ArticleId IdType="doi">10.1002/tox.22007</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list></list><tree><noCountry><name sortKey="Miller, Charles A" sort="Miller, Charles A" uniqKey="Miller C" first="Charles A" last="Miller">Charles A. Miller</name><name sortKey="Rando, Roy" sort="Rando, Roy" uniqKey="Rando R" first="Roy" last="Rando">Roy Rando</name><name sortKey="Sabbioni, Gabriele" sort="Sabbioni, Gabriele" uniqKey="Sabbioni G" first="Gabriele" last="Sabbioni">Gabriele Sabbioni</name><name sortKey="Wilson, Mark J" sort="Wilson, Mark J" uniqKey="Wilson M" first="Mark J" last="Wilson">Mark J. Wilson</name></noCountry></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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