Cytotoxic Effects of Environmental Toxins on Human Glial Cells.
Identifieur interne : 003D89 ( Ncbi/Merge ); précédent : 003D88; suivant : 003D90Cytotoxic Effects of Environmental Toxins on Human Glial Cells.
Auteurs : Fiona D'Mello [Australie] ; Nady Braidy [Australie] ; Helder Marçal [Australie] ; Gilles Guillemin [Australie] ; Fanny Rossi [France] ; Mirielle Chinian [Polynésie française] ; Dominique Laurent [France] ; Charles Teo [Australie] ; Brett A. Neilan [Australie]Source :
- Neurotoxicity research [ 1476-3524 ] ; 2017.
Descripteurs français
- KwdFr :
- Acide lipoïque (pharmacologie), Acides aminés diaminés (toxicité), Astrocytes (), Astrocytes (métabolisme), Calcium (métabolisme), Ciguatoxines (toxicité), Culture primaire de cellules, Dégénérescence nerveuse (), Espèces réactives de l'oxygène (métabolisme), Expression des gènes (), Humains, L-Lactate dehydrogenase (métabolisme), Microcystines (antagonistes et inhibiteurs), Microcystines (toxicité), Prolifération cellulaire (), Saxitoxine (toxicité).
- MESH :
- antagonistes et inhibiteurs : Microcystines.
- métabolisme : Astrocytes, Calcium, Espèces réactives de l'oxygène, L-Lactate dehydrogenase.
- pharmacologie : Acide lipoïque.
- toxicité : Acides aminés diaminés, Ciguatoxines, Microcystines, Saxitoxine.
- Astrocytes, Culture primaire de cellules, Dégénérescence nerveuse, Expression des gènes, Humains, Prolifération cellulaire.
English descriptors
- KwdEn :
- Amino Acids, Diamino (toxicity), Astrocytes (drug effects), Astrocytes (metabolism), Calcium (metabolism), Cell Proliferation (drug effects), Ciguatoxins (toxicity), Gene Expression (drug effects), Humans, L-Lactate Dehydrogenase (metabolism), Microcystins (antagonists & inhibitors), Microcystins (toxicity), Nerve Degeneration (chemically induced), Primary Cell Culture, Reactive Oxygen Species (metabolism), Saxitoxin (toxicity), Thioctic Acid (pharmacology).
- MESH :
- chemical , antagonists & inhibitors : Microcystins.
- chemical , metabolism : Calcium, L-Lactate Dehydrogenase, Reactive Oxygen Species.
- chemical , pharmacology : Thioctic Acid.
- chemical , toxicity : Amino Acids, Diamino, Ciguatoxins, Microcystins, Saxitoxin.
- chemically induced : Nerve Degeneration.
- drug effects : Astrocytes, Cell Proliferation, Gene Expression.
- metabolism : Astrocytes.
- Humans, Primary Cell Culture.
Abstract
Toxins produced by cyanobacteria and dinoflagellates have increasingly become a public health concern due to their degenerative effects on mammalian tissue and cells. In particular, emerging evidence has called attention to the neurodegenerative effects of the cyanobacterial toxin β-N-methylamino-L-alanine (BMAA). Other toxins such as the neurotoxins saxitoxin and ciguatoxin, as well as the hepatotoxic microcystin, have been previously shown to have a range of effects upon the nervous system. However, the capacity of these toxins to cause neurodegeneration in human cells has not, to our knowledge, been previously investigated. This study aimed to examine the cytotoxic effects of BMAA, microcystin-LR (MC-LR), saxitoxin (STX) and ciguatoxin (CTX-1B) on primary adult human astrocytes. We also demonstrated that α-lipoate attenuated MC-LR toxicity in primary astrocytes and characterised changes in gene expression which could potentially be caused by these toxins in primary astrocytes. Herein, we are the first to show that all of these toxins are capable of causing physiological changes consistent with neurodegeneration in glial cells, via oxidative stress and excitotoxicity, leading to a reduction in cell proliferation culminating in cell death. In addition, MC-LR toxicity was reduced significantly in astrocytes-treated α-lipoic acid. While there were no significant changes in gene expression, many of the probes that were altered were associated with neurodegenerative disease pathogenesis. Overall, this is important in advancing our current understanding of the mechanism of toxicity of MC-LR on human brain function in vitro, particularly in the context of neurodegeneration.
DOI: 10.1007/s12640-016-9678-5
PubMed: 27796937
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France.</nlm:affiliation><country xml:lang="fr">France</country><wicri:regionArea>Université de Toulouse, UPS, UMR-152 (Pharma-Dev), rte de Narbonne, cedex 9, F-31062, Toulouse</wicri:regionArea><placeName><region type="region" nuts="2">Occitanie (région administrative)</region><region type="old region" nuts="2">Midi-Pyrénées</region><settlement type="city">Toulouse</settlement></placeName></affiliation></author><author><name sortKey="Chinian, Mirielle" sort="Chinian, Mirielle" uniqKey="Chinian M" first="Mirielle" last="Chinian">Mirielle Chinian</name><affiliation wicri:level="1"><nlm:affiliation>Ecosystèmes Insulaires Océaniens UMR-241, Institut Louis Malardé, Laboratoire de recherche sur les Microalgues Toxiques, BP 30, 98713, Tahiti, Papeete, French Polynesia.</nlm:affiliation><country xml:lang="fr">Polynésie française</country><wicri:regionArea>Ecosystèmes Insulaires Océaniens UMR-241, Institut Louis Malardé, Laboratoire de recherche sur les Microalgues Toxiques, BP 30, 98713, Tahiti, Papeete</wicri:regionArea><wicri:noRegion>Papeete</wicri:noRegion></affiliation></author><author><name sortKey="Laurent, Dominique" sort="Laurent, Dominique" uniqKey="Laurent D" first="Dominique" last="Laurent">Dominique Laurent</name><affiliation wicri:level="3"><nlm:affiliation>Université de Toulouse, UPS, UMR-152 (Pharma-Dev), rte de Narbonne, cedex 9, F-31062, Toulouse, France.</nlm:affiliation><country xml:lang="fr">France</country><wicri:regionArea>Université de Toulouse, UPS, UMR-152 (Pharma-Dev), rte de Narbonne, cedex 9, F-31062, Toulouse</wicri:regionArea><placeName><settlement type="city">Toulouse</settlement><region type="region" nuts="2">Occitanie (région administrative)</region><region type="old region" nuts="2">Midi-Pyrénées</region></placeName></affiliation></author><author><name sortKey="Teo, Charles" sort="Teo, Charles" uniqKey="Teo C" first="Charles" last="Teo">Charles Teo</name><affiliation wicri:level="3"><nlm:affiliation>Minimally Invasive Cancer Centre, Prince of Wales Hospital, Sydney, Australia.</nlm:affiliation><country xml:lang="fr">Australie</country><wicri:regionArea>Minimally Invasive Cancer Centre, Prince of Wales Hospital, Sydney</wicri:regionArea><placeName><settlement type="city">Sydney</settlement><region type="état">Nouvelle-Galles du Sud</region></placeName></affiliation></author><author><name sortKey="Neilan, Brett A" sort="Neilan, Brett A" uniqKey="Neilan B" first="Brett A" last="Neilan">Brett A. Neilan</name><affiliation wicri:level="1"><nlm:affiliation>School of Biotechnology and Biomolecular Sciences, The University of New South Wales, Sydney, NSW, 2052, Australia. b.neilan@unsw.edu.au.</nlm:affiliation><country xml:lang="fr">Australie</country><wicri:regionArea>School of Biotechnology and Biomolecular Sciences, The University of New South Wales, Sydney, NSW, 2052</wicri:regionArea><wicri:noRegion>2052</wicri:noRegion></affiliation></author></analytic><series><title level="j">Neurotoxicity research</title><idno type="eISSN">1476-3524</idno><imprint><date when="2017" type="published">2017</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Amino Acids, Diamino (toxicity)</term><term>Astrocytes (drug effects)</term><term>Astrocytes (metabolism)</term><term>Calcium (metabolism)</term><term>Cell Proliferation (drug effects)</term><term>Ciguatoxins (toxicity)</term><term>Gene Expression (drug effects)</term><term>Humans</term><term>L-Lactate Dehydrogenase (metabolism)</term><term>Microcystins (antagonists & inhibitors)</term><term>Microcystins (toxicity)</term><term>Nerve Degeneration (chemically induced)</term><term>Primary Cell Culture</term><term>Reactive Oxygen Species (metabolism)</term><term>Saxitoxin (toxicity)</term><term>Thioctic Acid (pharmacology)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Acide lipoïque (pharmacologie)</term><term>Acides aminés diaminés (toxicité)</term><term>Astrocytes ()</term><term>Astrocytes (métabolisme)</term><term>Calcium (métabolisme)</term><term>Ciguatoxines (toxicité)</term><term>Culture primaire de cellules</term><term>Dégénérescence nerveuse ()</term><term>Espèces réactives de l'oxygène (métabolisme)</term><term>Expression des gènes ()</term><term>Humains</term><term>L-Lactate dehydrogenase (métabolisme)</term><term>Microcystines (antagonistes et inhibiteurs)</term><term>Microcystines (toxicité)</term><term>Prolifération cellulaire ()</term><term>Saxitoxine (toxicité)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="antagonists & inhibitors" xml:lang="en"><term>Microcystins</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Calcium</term><term>L-Lactate Dehydrogenase</term><term>Reactive Oxygen Species</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Thioctic Acid</term></keywords><keywords scheme="MESH" type="chemical" qualifier="toxicity" xml:lang="en"><term>Amino Acids, Diamino</term><term>Ciguatoxins</term><term>Microcystins</term><term>Saxitoxin</term></keywords><keywords scheme="MESH" qualifier="antagonistes et inhibiteurs" xml:lang="fr"><term>Microcystines</term></keywords><keywords scheme="MESH" qualifier="chemically induced" xml:lang="en"><term>Nerve Degeneration</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Astrocytes</term><term>Cell Proliferation</term><term>Gene Expression</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Astrocytes</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Astrocytes</term><term>Calcium</term><term>Espèces réactives de l'oxygène</term><term>L-Lactate dehydrogenase</term></keywords><keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Acide lipoïque</term></keywords><keywords scheme="MESH" qualifier="toxicité" xml:lang="fr"><term>Acides aminés diaminés</term><term>Ciguatoxines</term><term>Microcystines</term><term>Saxitoxine</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Humans</term><term>Primary Cell Culture</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Astrocytes</term><term>Culture primaire de cellules</term><term>Dégénérescence nerveuse</term><term>Expression des gènes</term><term>Humains</term><term>Prolifération cellulaire</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Toxins produced by cyanobacteria and dinoflagellates have increasingly become a public health concern due to their degenerative effects on mammalian tissue and cells. In particular, emerging evidence has called attention to the neurodegenerative effects of the cyanobacterial toxin β-N-methylamino-L-alanine (BMAA). Other toxins such as the neurotoxins saxitoxin and ciguatoxin, as well as the hepatotoxic microcystin, have been previously shown to have a range of effects upon the nervous system. However, the capacity of these toxins to cause neurodegeneration in human cells has not, to our knowledge, been previously investigated. This study aimed to examine the cytotoxic effects of BMAA, microcystin-LR (MC-LR), saxitoxin (STX) and ciguatoxin (CTX-1B) on primary adult human astrocytes. We also demonstrated that α-lipoate attenuated MC-LR toxicity in primary astrocytes and characterised changes in gene expression which could potentially be caused by these toxins in primary astrocytes. Herein, we are the first to show that all of these toxins are capable of causing physiological changes consistent with neurodegeneration in glial cells, via oxidative stress and excitotoxicity, leading to a reduction in cell proliferation culminating in cell death. In addition, MC-LR toxicity was reduced significantly in astrocytes-treated α-lipoic acid. While there were no significant changes in gene expression, many of the probes that were altered were associated with neurodegenerative disease pathogenesis. Overall, this is important in advancing our current understanding of the mechanism of toxicity of MC-LR on human brain function in vitro, particularly in the context of neurodegeneration.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">27796937</PMID><DateCreated><Year>2016</Year><Month>10</Month><Day>31</Day></DateCreated><DateCompleted><Year>2017</Year><Month>10</Month><Day>10</Day></DateCompleted><DateRevised><Year>2017</Year><Month>11</Month><Day>10</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1476-3524</ISSN><JournalIssue CitedMedium="Internet"><Volume>31</Volume><Issue>2</Issue><PubDate><Year>2017</Year><Month>Feb</Month></PubDate></JournalIssue><Title>Neurotoxicity research</Title><ISOAbbreviation>Neurotox Res</ISOAbbreviation></Journal><ArticleTitle>Cytotoxic Effects of Environmental Toxins on Human Glial Cells.</ArticleTitle><Pagination><MedlinePgn>245-258</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1007/s12640-016-9678-5</ELocationID><Abstract><AbstractText>Toxins produced by cyanobacteria and dinoflagellates have increasingly become a public health concern due to their degenerative effects on mammalian tissue and cells. In particular, emerging evidence has called attention to the neurodegenerative effects of the cyanobacterial toxin β-N-methylamino-L-alanine (BMAA). Other toxins such as the neurotoxins saxitoxin and ciguatoxin, as well as the hepatotoxic microcystin, have been previously shown to have a range of effects upon the nervous system. However, the capacity of these toxins to cause neurodegeneration in human cells has not, to our knowledge, been previously investigated. This study aimed to examine the cytotoxic effects of BMAA, microcystin-LR (MC-LR), saxitoxin (STX) and ciguatoxin (CTX-1B) on primary adult human astrocytes. We also demonstrated that α-lipoate attenuated MC-LR toxicity in primary astrocytes and characterised changes in gene expression which could potentially be caused by these toxins in primary astrocytes. Herein, we are the first to show that all of these toxins are capable of causing physiological changes consistent with neurodegeneration in glial cells, via oxidative stress and excitotoxicity, leading to a reduction in cell proliferation culminating in cell death. In addition, MC-LR toxicity was reduced significantly in astrocytes-treated α-lipoic acid. While there were no significant changes in gene expression, many of the probes that were altered were associated with neurodegenerative disease pathogenesis. Overall, this is important in advancing our current understanding of the mechanism of toxicity of MC-LR on human brain function in vitro, particularly in the context of neurodegeneration.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>D'Mello</LastName><ForeName>Fiona</ForeName><Initials>F</Initials><AffiliationInfo><Affiliation>School of Biotechnology and Biomolecular Sciences, The University of New South Wales, Sydney, NSW, 2052, Australia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Braidy</LastName><ForeName>Nady</ForeName><Initials>N</Initials><AffiliationInfo><Affiliation>Centre for Healthy Brain Ageing, School of Psychiatry, Faculty of Medicine, The University of New South Wales, Sydney, Australia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Marçal</LastName><ForeName>Helder</ForeName><Initials>H</Initials><AffiliationInfo><Affiliation>School of Biotechnology and Biomolecular Sciences, The University of New South Wales, Sydney, NSW, 2052, Australia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Guillemin</LastName><ForeName>Gilles</ForeName><Initials>G</Initials><AffiliationInfo><Affiliation>Faculty of Medicine and Health Science, Neuroinflammation group, Macquarie University, Sydney, Australia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Rossi</LastName><ForeName>Fanny</ForeName><Initials>F</Initials><AffiliationInfo><Affiliation>Université de Toulouse, UPS, UMR-152 (Pharma-Dev), rte de Narbonne, cedex 9, F-31062, Toulouse, France.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Institut de Recherche pour le Développement (IRD), UMR-152, BP 529, 98713, Tahiti, Papeete, French Polynesia.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Pacific Biotech SAS, BP 140 289, 98701, Tahiti, Arue, French Polynesia.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Ecosystèmes Insulaires Océaniens, UMR-241, Université de la Polynésie française, BP 6570, 98702, Tahiti, Faa'a, French Polynesia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Chinian</LastName><ForeName>Mirielle</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Ecosystèmes Insulaires Océaniens UMR-241, Institut Louis Malardé, Laboratoire de recherche sur les Microalgues Toxiques, BP 30, 98713, Tahiti, Papeete, French Polynesia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Laurent</LastName><ForeName>Dominique</ForeName><Initials>D</Initials><AffiliationInfo><Affiliation>Université de Toulouse, UPS, UMR-152 (Pharma-Dev), rte de Narbonne, cedex 9, F-31062, Toulouse, France.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Institut de Recherche pour le Développement (IRD), UMR-152, BP 529, 98713, Tahiti, Papeete, French Polynesia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Teo</LastName><ForeName>Charles</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>Minimally Invasive Cancer Centre, Prince of Wales Hospital, Sydney, Australia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Neilan</LastName><ForeName>Brett A</ForeName><Initials>BA</Initials><AffiliationInfo><Affiliation>School of Biotechnology and Biomolecular Sciences, The University of New South Wales, Sydney, NSW, 2052, Australia. b.neilan@unsw.edu.au.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2016</Year><Month>10</Month><Day>29</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Neurotox Res</MedlineTA><NlmUniqueID>100929017</NlmUniqueID><ISSNLinking>1029-8428</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000599">Amino Acids, Diamino</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D052998">Microcystins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D017382">Reactive Oxygen Species</NameOfSubstance></Chemical><Chemical><RegistryNumber>108SA6URTV</RegistryNumber><NameOfSubstance UI="C001824">beta-N-methylamino-L-alanine</NameOfSubstance></Chemical><Chemical><RegistryNumber>11050-21-8</RegistryNumber><NameOfSubstance UI="D002922">Ciguatoxins</NameOfSubstance></Chemical><Chemical><RegistryNumber>35523-89-8</RegistryNumber><NameOfSubstance UI="D012530">Saxitoxin</NameOfSubstance></Chemical><Chemical><RegistryNumber>73Y7P0K73Y</RegistryNumber><NameOfSubstance UI="D008063">Thioctic Acid</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 1.1.1.27</RegistryNumber><NameOfSubstance UI="D007770">L-Lactate Dehydrogenase</NameOfSubstance></Chemical><Chemical><RegistryNumber>EQ8332842Y</RegistryNumber><NameOfSubstance UI="C057862">cyanoginosin LR</NameOfSubstance></Chemical><Chemical><RegistryNumber>SY7Q814VUP</RegistryNumber><NameOfSubstance UI="D002118">Calcium</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><CommentsCorrectionsList><CommentsCorrections RefType="Cites"><RefSource>Ann N Y Acad Sci. 1989;568:234-51</RefSource><PMID Version="1">2576507</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Environ Toxicol. 2014 Mar;29(3):261-8</RefSource><PMID Version="1">22223477</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Acta Neurol Scand. 2004 Oct;110(4):267-9</RefSource><PMID Version="1">15355492</PMID></CommentsCorrections><CommentsCorrections 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Version="1">19254284</PMID></CommentsCorrections></CommentsCorrectionsList><MeshHeadingList><MeshHeading><DescriptorName UI="D000599" MajorTopicYN="N">Amino Acids, Diamino</DescriptorName><QualifierName UI="Q000633" MajorTopicYN="Y">toxicity</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D001253" MajorTopicYN="N">Astrocytes</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="Y">drug effects</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002118" MajorTopicYN="N">Calcium</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D049109" MajorTopicYN="N">Cell Proliferation</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002922" MajorTopicYN="N">Ciguatoxins</DescriptorName><QualifierName UI="Q000633" MajorTopicYN="Y">toxicity</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015870" MajorTopicYN="N">Gene Expression</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007770" MajorTopicYN="N">L-Lactate Dehydrogenase</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D052998" MajorTopicYN="N">Microcystins</DescriptorName><QualifierName UI="Q000037" MajorTopicYN="N">antagonists & inhibitors</QualifierName><QualifierName UI="Q000633" MajorTopicYN="Y">toxicity</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D009410" MajorTopicYN="N">Nerve Degeneration</DescriptorName><QualifierName UI="Q000139" MajorTopicYN="N">chemically induced</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D061251" MajorTopicYN="N">Primary Cell Culture</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D017382" MajorTopicYN="N">Reactive Oxygen Species</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D012530" MajorTopicYN="N">Saxitoxin</DescriptorName><QualifierName UI="Q000633" MajorTopicYN="Y">toxicity</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008063" MajorTopicYN="N">Thioctic Acid</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Cyanobacteria</Keyword><Keyword MajorTopicYN="N">Glial cells</Keyword><Keyword MajorTopicYN="N">Microcystin</Keyword><Keyword MajorTopicYN="N">Neurodegeneration</Keyword><Keyword MajorTopicYN="N">Neuroinflammation</Keyword><Keyword MajorTopicYN="N">Oxidative stress</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2016</Year><Month>01</Month><Day>12</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2016</Year><Month>10</Month><Day>14</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2016</Year><Month>09</Month><Day>29</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2016</Year><Month>11</Month><Day>1</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2017</Year><Month>10</Month><Day>11</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2016</Year><Month>11</Month><Day>1</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">27796937</ArticleId><ArticleId IdType="doi">10.1007/s12640-016-9678-5</ArticleId><ArticleId IdType="pii">10.1007/s12640-016-9678-5</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>Australie</li><li>France</li><li>Polynésie française</li></country><region><li>Midi-Pyrénées</li><li>Nouvelle-Galles du Sud</li><li>Occitanie (région administrative)</li></region><settlement><li>Sydney</li><li>Toulouse</li></settlement></list><tree><country name="Australie"><noRegion><name sortKey="D Mello, Fiona" sort="D Mello, Fiona" uniqKey="D Mello F" first="Fiona" last="D'Mello">Fiona D'Mello</name></noRegion><name sortKey="Braidy, Nady" sort="Braidy, Nady" uniqKey="Braidy N" first="Nady" last="Braidy">Nady Braidy</name><name sortKey="Guillemin, Gilles" sort="Guillemin, Gilles" uniqKey="Guillemin G" first="Gilles" last="Guillemin">Gilles Guillemin</name><name sortKey="Marcal, Helder" sort="Marcal, Helder" uniqKey="Marcal H" first="Helder" last="Marçal">Helder Marçal</name><name sortKey="Neilan, Brett A" sort="Neilan, Brett A" uniqKey="Neilan B" first="Brett A" last="Neilan">Brett A. Neilan</name><name sortKey="Teo, Charles" sort="Teo, Charles" uniqKey="Teo C" first="Charles" last="Teo">Charles Teo</name></country><country name="France"><region name="Occitanie (région administrative)"><name sortKey="Rossi, Fanny" sort="Rossi, Fanny" uniqKey="Rossi F" first="Fanny" last="Rossi">Fanny Rossi</name></region><name sortKey="Laurent, Dominique" sort="Laurent, Dominique" uniqKey="Laurent D" first="Dominique" last="Laurent">Dominique Laurent</name></country><country name="Polynésie française"><noRegion><name sortKey="Chinian, Mirielle" sort="Chinian, Mirielle" uniqKey="Chinian M" first="Mirielle" last="Chinian">Mirielle Chinian</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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