Cytotoxic Effects of Environmental Toxins on Human Glial Cells.
Identifieur interne : 003D89 ( Ncbi/Curation ); 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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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></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2017">2017</date><idno type="RBID">pubmed:27796937</idno><idno type="pmid">27796937</idno><idno type="doi">10.1007/s12640-016-9678-5</idno><idno type="wicri:Area/PubMed/Corpus">001172</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">001172</idno><idno type="wicri:Area/PubMed/Curation">001169</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Curation">001169</idno><idno 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uniqKey="Braidy N" first="Nady" last="Braidy">Nady Braidy</name><affiliation wicri:level="3"><nlm:affiliation>Centre for Healthy Brain Ageing, School of Psychiatry, Faculty of Medicine, The University of New South Wales, Sydney, Australia.</nlm:affiliation><country xml:lang="fr">Australie</country><wicri:regionArea>Centre for Healthy Brain Ageing, School of Psychiatry, Faculty of Medicine, The University of New South Wales, Sydney</wicri:regionArea><placeName><settlement type="city">Sydney</settlement><region type="état">Nouvelle-Galles du Sud</region></placeName></affiliation></author><author><name sortKey="Marcal, Helder" sort="Marcal, Helder" uniqKey="Marcal H" first="Helder" last="Marçal">Helder Marçal</name><affiliation wicri:level="1"><nlm:affiliation>School of Biotechnology and Biomolecular Sciences, The University of New South Wales, Sydney, NSW, 2052, Australia.</nlm:affiliation><country xml:lang="fr">Australie</country><wicri:regionArea>School of Biotechnology and 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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><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></record>Pour manipuler ce document sous Unix (Dilib)
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