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D'Mello F., Braidy N., Marcal H., Guillemin G., Rossi F., Chinian M., Laurent Dominique, Teo C., Neilan B. A. (2017). Cytotoxic effects of environmental toxins on human glial cells. Neurotoxicity Research, 31 (2), 245-258. ISSN 1029-8428

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Lien direct chez l'éditeur doi:10.1007/s12640-016-9678-5

Titre
Cytotoxic effects of environmental toxins on human glial cells
Année de publication2017
Type de documentArticle référencé dans le Web of Science WOS:000392307000005
AuteursD'Mello F., Braidy N., Marcal H., Guillemin G., Rossi F., Chinian M., Laurent Dominique, Teo C., Neilan B. A.
SourceNeurotoxicity Research, 2017, 31 (2), p. 245-258. ISSN 1029-8428
RésuméToxins 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 beta-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 alpha-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 alpha-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.
Plan de classementSubstances naturelles [035] ; Santé : généralités [050] ; Sciences fondamentales / Techniques d'analyse et de recherche [020]
LocalisationFonds IRD [F B010069606]
Identifiant IRDfdi:010069606
Lien permanenthttp://www.documentation.ird.fr/hor/fdi:010069606

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