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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<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>
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<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>
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<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>
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<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>
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<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>
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<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>
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