Role of Bim in diallyl trisulfide-induced cytotoxicity in human cancer cells.
Identifieur interne : 000920 ( Main/Exploration ); précédent : 000919; suivant : 000921Role of Bim in diallyl trisulfide-induced cytotoxicity in human cancer cells.
Auteurs : Byeong-Chel Lee [États-Unis] ; Bae-Hang Park ; Seog-Young Kim ; Yong J. LeeSource :
- Journal of cellular biochemistry [ 1097-4644 ] ; 2011.
Descripteurs français
- KwdFr :
- Ail (composition chimique), Antinéoplasiques (pharmacologie), Antinéoplasiques (toxicité), Antioxydants (pharmacologie), Antioxydants (toxicité), Apoptose (MeSH), Composés allyliques (pharmacologie), Composés allyliques (toxicité), Espèces réactives de l'oxygène (métabolisme), Humains (MeSH), JNK Mitogen-Activated Protein Kinases (métabolisme), Lignée cellulaire tumorale (MeSH), MAP Kinase Kinase Kinase 5 (métabolisme), Mitochondries (métabolisme), Protéine-11 analogue à Bcl-2 (MeSH), Protéines membranaires (métabolisme), Protéines proto-oncogènes (métabolisme), Protéines régulatrices de l'apoptose (métabolisme), Relation dose-effet des médicaments (MeSH), Sulfures (pharmacologie), Sulfures (toxicité), Survie cellulaire (effets des médicaments et des substances chimiques), Transduction du signal (MeSH).
- MESH :
- composition chimique : Ail.
- effets des médicaments et des substances chimiques : Survie cellulaire.
- métabolisme : Espèces réactives de l'oxygène, JNK Mitogen-Activated Protein Kinases, MAP Kinase Kinase Kinase 5, Mitochondries, Protéines membranaires, Protéines proto-oncogènes, Protéines régulatrices de l'apoptose.
- pharmacologie : Antinéoplasiques, Antioxydants, Composés allyliques, Sulfures.
- toxicité : Antinéoplasiques, Antioxydants, Composés allyliques, Sulfures.
- Apoptose, Humains, Lignée cellulaire tumorale, Protéine-11 analogue à Bcl-2, Relation dose-effet des médicaments, Transduction du signal.
English descriptors
- KwdEn :
- Allyl Compounds (pharmacology), Allyl Compounds (toxicity), Antineoplastic Agents (pharmacology), Antineoplastic Agents (toxicity), Antioxidants (pharmacology), Antioxidants (toxicity), Apoptosis (MeSH), Apoptosis Regulatory Proteins (metabolism), Bcl-2-Like Protein 11 (MeSH), Cell Line, Tumor (MeSH), Cell Survival (drug effects), Dose-Response Relationship, Drug (MeSH), Garlic (chemistry), Humans (MeSH), JNK Mitogen-Activated Protein Kinases (metabolism), MAP Kinase Kinase Kinase 5 (metabolism), Membrane Proteins (metabolism), Mitochondria (metabolism), Proto-Oncogene Proteins (metabolism), Reactive Oxygen Species (metabolism), Signal Transduction (MeSH), Sulfides (pharmacology), Sulfides (toxicity).
- MESH :
- chemical , metabolism : Apoptosis Regulatory Proteins, JNK Mitogen-Activated Protein Kinases, MAP Kinase Kinase Kinase 5, Membrane Proteins, Proto-Oncogene Proteins, Reactive Oxygen Species.
- chemical , pharmacology : Allyl Compounds, Antineoplastic Agents, Antioxidants, Sulfides.
- chemical , toxicity : Allyl Compounds, Antineoplastic Agents, Antioxidants, Sulfides.
- chemistry : Garlic.
- drug effects : Cell Survival.
- metabolism : Mitochondria.
- Apoptosis, Bcl-2-Like Protein 11, Cell Line, Tumor, Dose-Response Relationship, Drug, Humans, Signal Transduction.
Abstract
The aim of this study was to investigate the effect of garlic constituent diallyl trisulfide (DATS) on the cell-death signaling pathway in a human breast cell line (MDA-MB-231). We observed that DATS (10-100 µM) treatment resulted in dose- and time-dependent cytotoxicity. Treatment of MDA-MB-231 cells with a cytotoxicity inducing concentration of DATS (50-80 µM) resulted in an increase in the intracellular level of reactive oxygen species (ROS). Data from assay with MitoSOX(TM) Red reagent suggest that mitochondria are the main source of ROS generation during DATS treatment. DATS-induced oxidative stress was detected through glutaredoxin (GRX), a redox-sensing molecule, and subsequently GRX was dissociated from apoptosis signal-regulating kinase 1 (ASK1). Dissociation of GRX from ASK1 resulted in the activation of ASK1. ASK1 activated a downstream signal transduction JNK (c-Jun N-terminal kinase)-Bim pathway. SP600125, a JNK inhibitor, inhibited DATS-induced Bim phosphorylation and protected cells from DATS-induced cytotoxicity. Our results indicate that the cytotoxicity caused by DATS is mediated by the generation of ROS and subsequent activation of the ASK1-JNK-Bim signal transduction pathway in human breast carcinoma MDA-MB-231 cells.
DOI: 10.1002/jcb.22896
PubMed: 21053278
PubMed Central: PMC3010475
Affiliations:
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Le document en format XML
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Lee</name></author></analytic><series><title level="j">Journal of cellular biochemistry</title><idno type="eISSN">1097-4644</idno><imprint><date when="2011" type="published">2011</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Allyl Compounds (pharmacology)</term><term>Allyl Compounds (toxicity)</term><term>Antineoplastic Agents (pharmacology)</term><term>Antineoplastic Agents (toxicity)</term><term>Antioxidants (pharmacology)</term><term>Antioxidants (toxicity)</term><term>Apoptosis (MeSH)</term><term>Apoptosis Regulatory Proteins (metabolism)</term><term>Bcl-2-Like Protein 11 (MeSH)</term><term>Cell Line, Tumor (MeSH)</term><term>Cell Survival (drug effects)</term><term>Dose-Response Relationship, Drug (MeSH)</term><term>Garlic (chemistry)</term><term>Humans (MeSH)</term><term>JNK Mitogen-Activated Protein Kinases (metabolism)</term><term>MAP Kinase Kinase Kinase 5 (metabolism)</term><term>Membrane Proteins (metabolism)</term><term>Mitochondria (metabolism)</term><term>Proto-Oncogene Proteins (metabolism)</term><term>Reactive Oxygen Species (metabolism)</term><term>Signal Transduction (MeSH)</term><term>Sulfides (pharmacology)</term><term>Sulfides (toxicity)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Ail (composition chimique)</term><term>Antinéoplasiques (pharmacologie)</term><term>Antinéoplasiques (toxicité)</term><term>Antioxydants (pharmacologie)</term><term>Antioxydants (toxicité)</term><term>Apoptose (MeSH)</term><term>Composés allyliques (pharmacologie)</term><term>Composés allyliques (toxicité)</term><term>Espèces réactives de l'oxygène (métabolisme)</term><term>Humains (MeSH)</term><term>JNK Mitogen-Activated Protein Kinases (métabolisme)</term><term>Lignée cellulaire tumorale (MeSH)</term><term>MAP Kinase Kinase Kinase 5 (métabolisme)</term><term>Mitochondries (métabolisme)</term><term>Protéine-11 analogue à Bcl-2 (MeSH)</term><term>Protéines membranaires (métabolisme)</term><term>Protéines proto-oncogènes (métabolisme)</term><term>Protéines régulatrices de l'apoptose (métabolisme)</term><term>Relation dose-effet des médicaments (MeSH)</term><term>Sulfures (pharmacologie)</term><term>Sulfures (toxicité)</term><term>Survie cellulaire (effets des médicaments et des substances chimiques)</term><term>Transduction du signal (MeSH)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Apoptosis Regulatory Proteins</term><term>JNK Mitogen-Activated Protein Kinases</term><term>MAP Kinase Kinase Kinase 5</term><term>Membrane Proteins</term><term>Proto-Oncogene Proteins</term><term>Reactive Oxygen Species</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Allyl Compounds</term><term>Antineoplastic Agents</term><term>Antioxidants</term><term>Sulfides</term></keywords><keywords scheme="MESH" type="chemical" qualifier="toxicity" xml:lang="en"><term>Allyl Compounds</term><term>Antineoplastic Agents</term><term>Antioxidants</term><term>Sulfides</term></keywords><keywords scheme="MESH" qualifier="chemistry" xml:lang="en"><term>Garlic</term></keywords><keywords scheme="MESH" qualifier="composition chimique" xml:lang="fr"><term>Ail</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Cell Survival</term></keywords><keywords scheme="MESH" qualifier="effets des médicaments et des substances chimiques" xml:lang="fr"><term>Survie cellulaire</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Mitochondria</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Espèces réactives de l'oxygène</term><term>JNK Mitogen-Activated Protein Kinases</term><term>MAP Kinase Kinase Kinase 5</term><term>Mitochondries</term><term>Protéines membranaires</term><term>Protéines proto-oncogènes</term><term>Protéines régulatrices de l'apoptose</term></keywords><keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Antinéoplasiques</term><term>Antioxydants</term><term>Composés allyliques</term><term>Sulfures</term></keywords><keywords scheme="MESH" qualifier="toxicité" xml:lang="fr"><term>Antinéoplasiques</term><term>Antioxydants</term><term>Composés allyliques</term><term>Sulfures</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Apoptosis</term><term>Bcl-2-Like Protein 11</term><term>Cell Line, Tumor</term><term>Dose-Response Relationship, Drug</term><term>Humans</term><term>Signal Transduction</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Apoptose</term><term>Humains</term><term>Lignée cellulaire tumorale</term><term>Protéine-11 analogue à Bcl-2</term><term>Relation dose-effet des médicaments</term><term>Transduction du signal</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The aim of this study was to investigate the effect of garlic constituent diallyl trisulfide (DATS) on the cell-death signaling pathway in a human breast cell line (MDA-MB-231). We observed that DATS (10-100 µM) treatment resulted in dose- and time-dependent cytotoxicity. Treatment of MDA-MB-231 cells with a cytotoxicity inducing concentration of DATS (50-80 µM) resulted in an increase in the intracellular level of reactive oxygen species (ROS). Data from assay with MitoSOX(TM) Red reagent suggest that mitochondria are the main source of ROS generation during DATS treatment. DATS-induced oxidative stress was detected through glutaredoxin (GRX), a redox-sensing molecule, and subsequently GRX was dissociated from apoptosis signal-regulating kinase 1 (ASK1). Dissociation of GRX from ASK1 resulted in the activation of ASK1. ASK1 activated a downstream signal transduction JNK (c-Jun N-terminal kinase)-Bim pathway. SP600125, a JNK inhibitor, inhibited DATS-induced Bim phosphorylation and protected cells from DATS-induced cytotoxicity. Our results indicate that the cytotoxicity caused by DATS is mediated by the generation of ROS and subsequent activation of the ASK1-JNK-Bim signal transduction pathway in human breast carcinoma MDA-MB-231 cells.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">21053278</PMID><DateCompleted><Year>2011</Year><Month>07</Month><Day>19</Day></DateCompleted><DateRevised><Year>2018</Year><Month>11</Month><Day>13</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Electronic">1097-4644</ISSN><JournalIssue CitedMedium="Internet"><Volume>112</Volume><Issue>1</Issue><PubDate><Year>2011</Year><Month>Jan</Month></PubDate></JournalIssue><Title>Journal of cellular biochemistry</Title><ISOAbbreviation>J Cell Biochem</ISOAbbreviation></Journal><ArticleTitle>Role of Bim in diallyl trisulfide-induced cytotoxicity in human cancer cells.</ArticleTitle><Pagination><MedlinePgn>118-27</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1002/jcb.22896</ELocationID><Abstract><AbstractText>The aim of this study was to investigate the effect of garlic constituent diallyl trisulfide (DATS) on the cell-death signaling pathway in a human breast cell line (MDA-MB-231). We observed that DATS (10-100 µM) treatment resulted in dose- and time-dependent cytotoxicity. Treatment of MDA-MB-231 cells with a cytotoxicity inducing concentration of DATS (50-80 µM) resulted in an increase in the intracellular level of reactive oxygen species (ROS). Data from assay with MitoSOX(TM) Red reagent suggest that mitochondria are the main source of ROS generation during DATS treatment. DATS-induced oxidative stress was detected through glutaredoxin (GRX), a redox-sensing molecule, and subsequently GRX was dissociated from apoptosis signal-regulating kinase 1 (ASK1). Dissociation of GRX from ASK1 resulted in the activation of ASK1. ASK1 activated a downstream signal transduction JNK (c-Jun N-terminal kinase)-Bim pathway. SP600125, a JNK inhibitor, inhibited DATS-induced Bim phosphorylation and protected cells from DATS-induced cytotoxicity. Our results indicate that the cytotoxicity caused by DATS is mediated by the generation of ROS and subsequent activation of the ASK1-JNK-Bim signal transduction pathway in human breast carcinoma MDA-MB-231 cells.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Lee</LastName><ForeName>Byeong-Chel</ForeName><Initials>BC</Initials><AffiliationInfo><Affiliation>Department of Medicine, University of Pittsburgh, Pittsburgh, PA 15213, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Park</LastName><ForeName>Bae-Hang</ForeName><Initials>BH</Initials></Author><Author ValidYN="Y"><LastName>Kim</LastName><ForeName>Seog-Young</ForeName><Initials>SY</Initials></Author><Author ValidYN="Y"><LastName>Lee</LastName><ForeName>Yong J</ForeName><Initials>YJ</Initials></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>R01 CA140554-02</GrantID><Acronym>CA</Acronym><Agency>NCI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>CA121395</GrantID><Acronym>CA</Acronym><Agency>NCI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 CA140554</GrantID><Acronym>CA</Acronym><Agency>NCI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R03 CA121395</GrantID><Acronym>CA</Acronym><Agency>NCI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>CA140554</GrantID><Acronym>CA</Acronym><Agency>NCI NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D052061">Research Support, N.I.H., Extramural</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>J Cell Biochem</MedlineTA><NlmUniqueID>8205768</NlmUniqueID><ISSNLinking>0730-2312</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000498">Allyl Compounds</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000970">Antineoplastic Agents</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000975">Antioxidants</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D051017">Apoptosis Regulatory Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C000606775">BCL2L11 protein, human</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000072224">Bcl-2-Like Protein 11</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D008565">Membrane Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D011518">Proto-Oncogene Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D017382">Reactive Oxygen Species</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D013440">Sulfides</NameOfSubstance></Chemical><Chemical><RegistryNumber>0ZO1U5A3XX</RegistryNumber><NameOfSubstance UI="C042577">diallyl trisulfide</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.7.11.24</RegistryNumber><NameOfSubstance UI="D048031">JNK Mitogen-Activated Protein Kinases</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.7.11.25</RegistryNumber><NameOfSubstance UI="D048848">MAP Kinase Kinase Kinase 5</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.7.11.25</RegistryNumber><NameOfSubstance UI="C482858">MAP3K5 protein, human</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000498" MajorTopicYN="N">Allyl Compounds</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName><QualifierName UI="Q000633" MajorTopicYN="Y">toxicity</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000970" MajorTopicYN="N">Antineoplastic Agents</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName><QualifierName UI="Q000633" MajorTopicYN="Y">toxicity</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000975" MajorTopicYN="N">Antioxidants</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName><QualifierName UI="Q000633" MajorTopicYN="Y">toxicity</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D017209" MajorTopicYN="N">Apoptosis</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D051017" MajorTopicYN="N">Apoptosis Regulatory Proteins</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000072224" MajorTopicYN="N">Bcl-2-Like Protein 11</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D045744" MajorTopicYN="N">Cell Line, Tumor</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002470" MajorTopicYN="N">Cell Survival</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D004305" MajorTopicYN="N">Dose-Response Relationship, Drug</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005737" MajorTopicYN="N">Garlic</DescriptorName><QualifierName UI="Q000737" MajorTopicYN="N">chemistry</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D048031" MajorTopicYN="N">JNK Mitogen-Activated Protein Kinases</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D048848" MajorTopicYN="N">MAP Kinase Kinase Kinase 5</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008565" MajorTopicYN="N">Membrane Proteins</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008928" MajorTopicYN="N">Mitochondria</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D011518" MajorTopicYN="N">Proto-Oncogene Proteins</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D017382" MajorTopicYN="N">Reactive Oxygen Species</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015398" MajorTopicYN="N">Signal Transduction</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D013440" MajorTopicYN="N">Sulfides</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName><QualifierName UI="Q000633" MajorTopicYN="Y">toxicity</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="entrez"><Year>2010</Year><Month>11</Month><Day>6</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2010</Year><Month>11</Month><Day>6</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2011</Year><Month>7</Month><Day>20</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">21053278</ArticleId><ArticleId 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IdType="pubmed">9564042</ArticleId></ArticleIdList></Reference></ReferenceList></PubmedData></pubmed><affiliations><list><country><li>États-Unis</li></country><region><li>Pennsylvanie</li></region><settlement><li>Pittsburgh</li></settlement><orgName><li>Université de Pittsburgh</li></orgName></list><tree><noCountry><name sortKey="Kim, Seog Young" sort="Kim, Seog Young" uniqKey="Kim S" first="Seog-Young" last="Kim">Seog-Young Kim</name><name sortKey="Lee, Yong J" sort="Lee, Yong J" uniqKey="Lee Y" first="Yong J" last="Lee">Yong J. Lee</name><name sortKey="Park, Bae Hang" sort="Park, Bae Hang" uniqKey="Park B" first="Bae-Hang" last="Park">Bae-Hang Park</name></noCountry><country name="États-Unis"><region name="Pennsylvanie"><name sortKey="Lee, Byeong Chel" sort="Lee, Byeong Chel" uniqKey="Lee B" first="Byeong-Chel" last="Lee">Byeong-Chel Lee</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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