title: The ribotoxin deoxynivalenol affects the viability and functions of glial cells.
abstract: Glial cells are responsible for maintaining brain homeostasis. Modification of the viability and functions of glial cells, including astrocytes and microglia, are associated with neuronal death and neurological diseases. Many toxins (heavy metals, pesticides, bacterial or viral toxins) are known to impact on brain cell viability and functions. Although recent publications suggest a potential link between environmental exposure of humans to mycotoxins and neurological diseases, data regarding the effects of fungal toxins on brain cells are scarce. In the present study, we looked at the impact of deoxynivalenol (DON), a fungal ribotoxin, on glial cells from animal and human origin. We found that DON decreased the viability of glial cells with a higher toxicity against microglial cells compared with astrocytes. In addition to cellular toxicity, DON affected key functions of glial cells. Thus, DON caused a biphasic effect on the neuroinflammatory response of microglia to lipopolysaccharide (LPS), while sublethal doses of DON increased the LPS-induced secretion of TNF-α and nitric oxide, toxic doses inhibited it. In addition to affecting microglial functions, sublethal doses of DON also suppressed the uptake of L-glutamate by astrocytes. This inhibition was associated with a modification of the expression of the glutamate transporters at the plasma membrane. Our results suggest that environmental ribotoxins such as DON could, at low doses, cause modifications of brain homeostasis and possibly participate in the etiology of neurological diseases in which alterations of the glia are involved.
authors: CRN2M, CNRS UMR 6231, INRA USC 2027, University of Aix-Marseille 2 and Aix-Marseille 3, Faculté des Sciences de St-Jérôme, 13397 Marseille Cedex 20, France.
authors: Helisoa
authors: H
authors: Razafimanjato
authors: Amal
authors: A
authors: Benzaria
authors: Nadira
authors: N
authors: Taïeb
authors: Xiao-Jun
authors: XJ
authors: Guo
authors: Nicolas
authors: N
authors: Vidal
authors: Coralie
authors: C
authors: Di Scala
authors: Karine
authors: K
authors: Varini
authors: Marc
authors: M
authors: Maresca
mesh_terms: D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D001253:Astrocytes / Q000187:drug effects / Q000378:metabolism / Q000502:physiology; D015153:Blotting, Western; D002470:Cell Survival / Q000187:drug effects / Q000502:physiology; D002478:Cells, Cultured; D016207:Cytokines / Q000378:metabolism; D005974:Glutamate-Ammonia Ligase / Q000378:metabolism; D018698:Glutamic Acid / Q000378:metabolism; D006706:Homeostasis / Q000187:drug effects; D007249:Inflammation / Q000139:chemically induced / Q000473:pathology; D008070:Lipopolysaccharides / Q000633:toxicity; D008565:Membrane Proteins / Q000096:biosynthesis; D008856:Microscopy, Fluorescence; D009457:Neuroglia / Q000187:drug effects* / Q000502:physiology*; D009569:Nitric Oxide / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D014255:Trichothecenes / Q000633:toxicity*; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D016207:Cytokines; D008070:Lipopolysaccharides; D008565:Membrane Proteins; D014255:Trichothecenes; D014409:Tumor Necrosis Factor-alpha; D009569:Nitric Oxide; D018698:Glutamic Acid; D000255:Adenosine Triphosphate; D005974:Glutamate-Ammonia Ligase; C007262:deoxynivalenol