Isopulegol Mitigates Hyperglycemia Mediated Oxidative and Endoplasmic Reticulum Stress in HFD/STZ Induced Diabetic Rats.
Identifieur interne : 000026 ( Main/Exploration ); précédent : 000025; suivant : 000027Isopulegol Mitigates Hyperglycemia Mediated Oxidative and Endoplasmic Reticulum Stress in HFD/STZ Induced Diabetic Rats.
Auteurs : Chandrasekaran Sankaranarayanan [Inde] ; Karunanithi Kalaivani [Inde]Source :
- Archives of medical research [ 1873-5487 ] ; 2020.
Descripteurs français
- KwdFr :
- Acide ascorbique (sang), Animaux (MeSH), Antioxydants (pharmacologie), Catalase (métabolisme), Diabète expérimental (traitement médicamenteux), Glutathion (sang), Glutathione peroxidase (métabolisme), Glutathione reductase (métabolisme), Glutathione transferase (métabolisme), Glycémie (métabolisme), Hyperglycémie (anatomopathologie), Hypoglycémiants (pharmacologie), Insuline (sang), Mâle (MeSH), Peroxydation lipidique (effets des médicaments et des substances chimiques), Peroxydes lipidiques (sang), Rat Wistar (MeSH), Rats (MeSH), Streptozocine (MeSH), Stress du réticulum endoplasmique (effets des médicaments et des substances chimiques), Stress oxydatif (effets des médicaments et des substances chimiques), Substances réactives à l'acide thiobarbiturique (analyse), Superoxide dismutase (métabolisme), Vitamine E (sang).
- MESH :
- analyse : Substances réactives à l'acide thiobarbiturique.
- anatomopathologie : Hyperglycémie.
- effets des médicaments et des substances chimiques : Peroxydation lipidique, Stress du réticulum endoplasmique, Stress oxydatif.
- métabolisme : Catalase, Glutathione peroxidase, Glutathione reductase, Glutathione transferase, Glycémie, Superoxide dismutase.
- pharmacologie : Antioxydants, Hypoglycémiants.
- sang : Acide ascorbique, Glutathion, Insuline, Peroxydes lipidiques, Vitamine E.
- traitement médicamenteux : Diabète expérimental.
- Animaux, Mâle, Rat Wistar, Rats, Streptozocine.
English descriptors
- KwdEn :
- Animals (MeSH), Antioxidants (pharmacology), Ascorbic Acid (blood), Blood Glucose (metabolism), Catalase (metabolism), Cyclohexane Monoterpenes (pharmacology), Diabetes Mellitus, Experimental (drug therapy), Endoplasmic Reticulum Stress (drug effects), Glutathione (blood), Glutathione Peroxidase (metabolism), Glutathione Reductase (metabolism), Glutathione Transferase (metabolism), Hyperglycemia (pathology), Hypoglycemic Agents (pharmacology), Insulin (blood), Lipid Peroxidation (drug effects), Lipid Peroxides (blood), Male (MeSH), Oxidative Stress (drug effects), Rats (MeSH), Rats, Wistar (MeSH), Streptozocin (MeSH), Superoxide Dismutase (metabolism), Thiobarbituric Acid Reactive Substances (analysis), Vitamin E (blood).
- MESH :
- chemical , analysis : Thiobarbituric Acid Reactive Substances.
- chemical , blood : Ascorbic Acid, Glutathione, Insulin, Lipid Peroxides, Vitamin E.
- chemical , metabolism : Blood Glucose, Catalase, Glutathione Peroxidase, Glutathione Reductase, Glutathione Transferase, Superoxide Dismutase.
- chemical , pharmacology : Antioxidants, Cyclohexane Monoterpenes, Hypoglycemic Agents.
- drug effects : Endoplasmic Reticulum Stress, Lipid Peroxidation, Oxidative Stress.
- drug therapy : Diabetes Mellitus, Experimental.
- pathology : Hyperglycemia.
- Animals, Male, Rats, Rats, Wistar, Streptozocin.
Abstract
BACKGROUND
Oxidative and endoplasmic reticulum stresses contribute to the pathogenesis of β-cell dysfunction in diabetes mellitus. This study investigates the effect of isopulegol on the above stresses in HFD/STZ induced diabetic rats.
METHODS
Animals in group I and II were placed in normal pellet diet and group II was treated with isopulegol at 200 mg/kg b.w. Animals in groups III-V were placed in HFD for 4 weeks and made diabetic with single intraperitoneal injection of STZ (35 mg/kg b.w) in 0.1 M citrate buffer (pH 4.5). Group III served as diabetic control while animals in group IV and V were treated with isopulegol (100 mg/kg b.w) and metformin (25 mg/kg b.w) respectively for 28 d.
RESULTS
The activities of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), glutathione sulphur transferase (GST), glutathione reductase (GR) and the levels of vitamin-E, vitamin-C, reduced glutathione (GSH) were significantly (p <0.05) decreased in plasma and tissues of diabetic rats. Thiobarbituric acid reactive acid substances (TBARS) and lipid hydroperoxides (LHP), indices of lipid peroxidation were also significantly (p <0.05) increased in diabetic rats. In pancreatic tissue ER stress markers PERK, elf2α, ATF4 and in hepatic tissue oxidative stress marker UCP-2 expression was significantly (p <1.0) increased in diabetic rats. Administration of isopulegol significantly improved antioxidant status and decreased oxidative and ER stress markers in diabetic treated rats. Histopathological studies on liver and kidney supported the above findings. The results are comparable with the standard drug metformin.
CONCLUSIONS
Isopulegol a naturally occurring monoterpene alcohol attenuated oxidative and ER stress in HFD/STZ induced diabetic rats.
DOI: 10.1016/j.arcmed.2020.02.001
PubMed: 32111490
Affiliations:
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(MeSH)</term><term>Streptozocin (MeSH)</term><term>Superoxide Dismutase (metabolism)</term><term>Thiobarbituric Acid Reactive Substances (analysis)</term><term>Vitamin E (blood)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Acide ascorbique (sang)</term><term>Animaux (MeSH)</term><term>Antioxydants (pharmacologie)</term><term>Catalase (métabolisme)</term><term>Diabète expérimental (traitement médicamenteux)</term><term>Glutathion (sang)</term><term>Glutathione peroxidase (métabolisme)</term><term>Glutathione reductase (métabolisme)</term><term>Glutathione transferase (métabolisme)</term><term>Glycémie (métabolisme)</term><term>Hyperglycémie (anatomopathologie)</term><term>Hypoglycémiants (pharmacologie)</term><term>Insuline (sang)</term><term>Mâle (MeSH)</term><term>Peroxydation lipidique (effets des médicaments et des substances chimiques)</term><term>Peroxydes lipidiques (sang)</term><term>Rat Wistar (MeSH)</term><term>Rats (MeSH)</term><term>Streptozocine (MeSH)</term><term>Stress du réticulum endoplasmique (effets des médicaments et des substances chimiques)</term><term>Stress oxydatif (effets des médicaments et des substances chimiques)</term><term>Substances réactives à l'acide thiobarbiturique (analyse)</term><term>Superoxide dismutase (métabolisme)</term><term>Vitamine E (sang)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="analysis" xml:lang="en"><term>Thiobarbituric Acid Reactive Substances</term></keywords><keywords scheme="MESH" type="chemical" qualifier="blood" xml:lang="en"><term>Ascorbic Acid</term><term>Glutathione</term><term>Insulin</term><term>Lipid Peroxides</term><term>Vitamin E</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Blood Glucose</term><term>Catalase</term><term>Glutathione Peroxidase</term><term>Glutathione Reductase</term><term>Glutathione Transferase</term><term>Superoxide Dismutase</term></keywords><keywords scheme="MESH" 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Wistar</term><term>Rats</term><term>Streptozocine</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p><b>BACKGROUND</b></p><p>Oxidative and endoplasmic reticulum stresses contribute to the pathogenesis of β-cell dysfunction in diabetes mellitus. This study investigates the effect of isopulegol on the above stresses in HFD/STZ induced diabetic rats.</p></div><div type="abstract" xml:lang="en"><p><b>METHODS</b></p><p>Animals in group I and II were placed in normal pellet diet and group II was treated with isopulegol at 200 mg/kg b.w. Animals in groups III-V were placed in HFD for 4 weeks and made diabetic with single intraperitoneal injection of STZ (35 mg/kg b.w) in 0.1 M citrate buffer (pH 4.5). Group III served as diabetic control while animals in group IV and V were treated with isopulegol (100 mg/kg b.w) and metformin (25 mg/kg b.w) respectively for 28 d.</p></div><div type="abstract" xml:lang="en"><p><b>RESULTS</b></p><p>The activities of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), glutathione sulphur transferase (GST), glutathione reductase (GR) and the levels of vitamin-E, vitamin-C, reduced glutathione (GSH) were significantly (p <0.05) decreased in plasma and tissues of diabetic rats. Thiobarbituric acid reactive acid substances (TBARS) and lipid hydroperoxides (LHP), indices of lipid peroxidation were also significantly (p <0.05) increased in diabetic rats. In pancreatic tissue ER stress markers PERK, elf2α, ATF4 and in hepatic tissue oxidative stress marker UCP-2 expression was significantly (p <1.0) increased in diabetic rats. Administration of isopulegol significantly improved antioxidant status and decreased oxidative and ER stress markers in diabetic treated rats. Histopathological studies on liver and kidney supported the above findings. The results are comparable with the standard drug metformin.</p></div><div type="abstract" xml:lang="en"><p><b>CONCLUSIONS</b></p><p>Isopulegol a naturally occurring monoterpene alcohol attenuated oxidative and ER stress in HFD/STZ induced diabetic rats.</p></div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" IndexingMethod="Curated" Owner="NLM"><PMID Version="1">32111490</PMID><DateCompleted><Year>2020</Year><Month>09</Month><Day>21</Day></DateCompleted><DateRevised><Year>2020</Year><Month>09</Month><Day>21</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1873-5487</ISSN><JournalIssue CitedMedium="Internet"><Volume>51</Volume><Issue>3</Issue><PubDate><Year>2020</Year><Month>04</Month></PubDate></JournalIssue><Title>Archives of medical research</Title><ISOAbbreviation>Arch Med Res</ISOAbbreviation></Journal><ArticleTitle>Isopulegol Mitigates Hyperglycemia Mediated Oxidative and Endoplasmic Reticulum Stress in HFD/STZ Induced Diabetic Rats.</ArticleTitle><Pagination><MedlinePgn>204-214</MedlinePgn></Pagination><ELocationID EIdType="pii" ValidYN="Y">S0188-4409(19)30319-4</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.arcmed.2020.02.001</ELocationID><Abstract><AbstractText Label="BACKGROUND">Oxidative and endoplasmic reticulum stresses contribute to the pathogenesis of β-cell dysfunction in diabetes mellitus. This study investigates the effect of isopulegol on the above stresses in HFD/STZ induced diabetic rats.</AbstractText><AbstractText Label="METHODS">Animals in group I and II were placed in normal pellet diet and group II was treated with isopulegol at 200 mg/kg b.w. Animals in groups III-V were placed in HFD for 4 weeks and made diabetic with single intraperitoneal injection of STZ (35 mg/kg b.w) in 0.1 M citrate buffer (pH 4.5). Group III served as diabetic control while animals in group IV and V were treated with isopulegol (100 mg/kg b.w) and metformin (25 mg/kg b.w) respectively for 28 d.</AbstractText><AbstractText Label="RESULTS">The activities of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), glutathione sulphur transferase (GST), glutathione reductase (GR) and the levels of vitamin-E, vitamin-C, reduced glutathione (GSH) were significantly (p <0.05) decreased in plasma and tissues of diabetic rats. Thiobarbituric acid reactive acid substances (TBARS) and lipid hydroperoxides (LHP), indices of lipid peroxidation were also significantly (p <0.05) increased in diabetic rats. In pancreatic tissue ER stress markers PERK, elf2α, ATF4 and in hepatic tissue oxidative stress marker UCP-2 expression was significantly (p <1.0) increased in diabetic rats. Administration of isopulegol significantly improved antioxidant status and decreased oxidative and ER stress markers in diabetic treated rats. Histopathological studies on liver and kidney supported the above findings. The results are comparable with the standard drug metformin.</AbstractText><AbstractText Label="CONCLUSIONS">Isopulegol a naturally occurring monoterpene alcohol attenuated oxidative and ER stress in HFD/STZ induced diabetic rats.</AbstractText><CopyrightInformation>Copyright © 2020 IMSS. Published by Elsevier Inc. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Sankaranarayanan</LastName><ForeName>Chandrasekaran</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>Department of Biochemistry and Biotechnology, Annamalai University, Annamalainagar, Tamilnadu, India. Electronic address: sankarhari05@gmail.com.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kalaivani</LastName><ForeName>Karunanithi</ForeName><Initials>K</Initials><AffiliationInfo><Affiliation>Department of Biochemistry and Biotechnology, Annamalai University, Annamalainagar, Tamilnadu, India.</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>2020</Year><Month>02</Month><Day>26</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Arch Med Res</MedlineTA><NlmUniqueID>9312706</NlmUniqueID><ISSNLinking>0188-4409</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000975">Antioxidants</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D001786">Blood Glucose</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000081005">Cyclohexane Monoterpenes</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D007004">Hypoglycemic Agents</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D007328">Insulin</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D008054">Lipid Peroxides</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D017392">Thiobarbituric Acid Reactive Substances</NameOfSubstance></Chemical><Chemical><RegistryNumber>1406-18-4</RegistryNumber><NameOfSubstance UI="D014810">Vitamin E</NameOfSubstance></Chemical><Chemical><RegistryNumber>3TH92O3BXN</RegistryNumber><NameOfSubstance UI="C409816">isopulegol</NameOfSubstance></Chemical><Chemical><RegistryNumber>5W494URQ81</RegistryNumber><NameOfSubstance UI="D013311">Streptozocin</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 1.11.1.6</RegistryNumber><NameOfSubstance UI="D002374">Catalase</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 1.11.1.9</RegistryNumber><NameOfSubstance UI="D005979">Glutathione Peroxidase</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 1.15.1.1</RegistryNumber><NameOfSubstance UI="D013482">Superoxide Dismutase</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 1.8.1.7</RegistryNumber><NameOfSubstance UI="D005980">Glutathione Reductase</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.5.1.18</RegistryNumber><NameOfSubstance UI="D005982">Glutathione Transferase</NameOfSubstance></Chemical><Chemical><RegistryNumber>GAN16C9B8O</RegistryNumber><NameOfSubstance UI="D005978">Glutathione</NameOfSubstance></Chemical><Chemical><RegistryNumber>PQ6CK8PD0R</RegistryNumber><NameOfSubstance UI="D001205">Ascorbic Acid</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000975" MajorTopicYN="N">Antioxidants</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="Y">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D001205" MajorTopicYN="N">Ascorbic Acid</DescriptorName><QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D001786" MajorTopicYN="N">Blood Glucose</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002374" MajorTopicYN="N">Catalase</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000081005" MajorTopicYN="N">Cyclohexane Monoterpenes</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="Y">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D003921" MajorTopicYN="N">Diabetes Mellitus, Experimental</DescriptorName><QualifierName UI="Q000188" MajorTopicYN="Y">drug therapy</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D059865" MajorTopicYN="N">Endoplasmic Reticulum Stress</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="Y">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005978" MajorTopicYN="N">Glutathione</DescriptorName><QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005979" MajorTopicYN="N">Glutathione Peroxidase</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005980" MajorTopicYN="N">Glutathione Reductase</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005982" MajorTopicYN="N">Glutathione Transferase</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006943" MajorTopicYN="N">Hyperglycemia</DescriptorName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D007004" MajorTopicYN="N">Hypoglycemic Agents</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="Y">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D007328" MajorTopicYN="N">Insulin</DescriptorName><QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015227" MajorTopicYN="N">Lipid Peroxidation</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008054" MajorTopicYN="N">Lipid Peroxides</DescriptorName><QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D018384" MajorTopicYN="N">Oxidative Stress</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="Y">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051381" MajorTopicYN="N">Rats</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D017208" MajorTopicYN="N">Rats, Wistar</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D013311" MajorTopicYN="N">Streptozocin</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D013482" MajorTopicYN="N">Superoxide Dismutase</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D017392" MajorTopicYN="N">Thiobarbituric Acid Reactive Substances</DescriptorName><QualifierName UI="Q000032" MajorTopicYN="N">analysis</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D014810" MajorTopicYN="N">Vitamin E</DescriptorName><QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="Y">Activated transcription factor 4 (ATF4)</Keyword><Keyword MajorTopicYN="Y">Eukaryotic initiation factor 2 alpha (eIF2α)</Keyword><Keyword MajorTopicYN="Y">Isopulegol</Keyword><Keyword MajorTopicYN="Y">Pancreatic endoplasmic reticulum kinase (PERK)</Keyword><Keyword MajorTopicYN="Y">Uncoupled protein 2 (UCP2)</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2019</Year><Month>03</Month><Day>20</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2020</Year><Month>01</Month><Day>20</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2020</Year><Month>02</Month><Day>10</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2020</Year><Month>3</Month><Day>1</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2020</Year><Month>9</Month><Day>22</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2020</Year><Month>3</Month><Day>1</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">32111490</ArticleId><ArticleId IdType="pii">S0188-4409(19)30319-4</ArticleId><ArticleId IdType="doi">10.1016/j.arcmed.2020.02.001</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>Inde</li></country></list><tree><country name="Inde"><noRegion><name sortKey="Sankaranarayanan, Chandrasekaran" sort="Sankaranarayanan, Chandrasekaran" uniqKey="Sankaranarayanan C" first="Chandrasekaran" last="Sankaranarayanan">Chandrasekaran Sankaranarayanan</name></noRegion><name sortKey="Kalaivani, Karunanithi" sort="Kalaivani, Karunanithi" uniqKey="Kalaivani K" first="Karunanithi" last="Kalaivani">Karunanithi Kalaivani</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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