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Tytuł pozycji:

SN56 neuronal cell death after 24 h and 14 days chlorpyrifos exposure through glutamate transmission dysfunction, increase of GSK-3β enzyme, β-amyloid and tau protein levels.

Tytuł :
SN56 neuronal cell death after 24 h and 14 days chlorpyrifos exposure through glutamate transmission dysfunction, increase of GSK-3β enzyme, β-amyloid and tau protein levels.
Autorzy :
Moyano P; Department of Toxicology and Legal Medicine, Medicine School, Complutense University of Madrid, 28041, Madrid, Spain.
Frejo MT; Department of Toxicology and Pharmacology, Veterinary Medicine School, Complutense University of Madrid, 28040, Madrid, Spain.
Anadon MJ; Department of Toxicology and Legal Medicine, Medicine School, Complutense University of Madrid, 28041, Madrid, Spain.
García JM; Department of Toxicology and Legal Medicine, Medicine School, Complutense University of Madrid, 28041, Madrid, Spain.
Díaz MJ; Department of Toxicology and Pharmacology, Veterinary Medicine School, Complutense University of Madrid, 28040, Madrid, Spain.
Lobo M; Department of Toxicology and Pharmacology, Veterinary Medicine School, Complutense University of Madrid, 28040, Madrid, Spain.
Sola E; Department of Pathology, Medicine School, Complutense University of Madrid, 28041, Madrid, Spain.
García J; Department of Toxicology and Legal Medicine, Medicine School, Complutense University of Madrid, 28041, Madrid, Spain.
Del Pino J; Department of Toxicology and Pharmacology, Veterinary Medicine School, Complutense University of Madrid, 28040, Madrid, Spain. Electronic address: .
Pokaż więcej
Źródło :
Toxicology [Toxicology] 2018 Jun 01; Vol. 402-403, pp. 17-27. Date of Electronic Publication: 2018 Apr 14.
Typ publikacji :
Journal Article; Research Support, Non-U.S. Gov't
Język :
English
Imprint Name(s) :
Publication: Limerick : Elsevier
Original Publication: Amsterdam. Elsevier/North-Holland.
MeSH Terms :
Amyloid beta-Peptides/*biosynthesis
Chlorpyrifos/*toxicity
Glutamic Acid/*metabolism
Glycogen Synthase Kinase 3 beta/*biosynthesis
Neurons/*metabolism
tau Proteins/*biosynthesis
Animals ; Cell Death/drug effects ; Cell Death/physiology ; Cell Line, Tumor ; Cell Survival/drug effects ; Cell Survival/physiology ; Dose-Response Relationship, Drug ; Insecticides/toxicity ; Mice ; Neurons/drug effects ; Synaptic Transmission/drug effects ; Synaptic Transmission/physiology ; Time Factors
Contributed Indexing :
Keywords: Aβ*; Basal forebrain neurons*; Cell death*; Chlorpyrifos*; GSK-3β*; Glutamate*; Tau*
Substance Nomenclature :
0 (Amyloid beta-Peptides)
0 (Insecticides)
0 (tau Proteins)
3KX376GY7L (Glutamic Acid)
EC 2.7.11.1 (Glycogen Synthase Kinase 3 beta)
JCS58I644W (Chlorpyrifos)
Entry Date(s) :
Date Created: 20180418 Date Completed: 20190128 Latest Revision: 20190128
Update Code :
20201218
DOI :
10.1016/j.tox.2018.04.003
PMID :
29665406
Czasopismo naukowe
Chlorpyrifos (CPF) is an organophosphate insecticide described to induce cognitive disorders, both after acute and repeated administration. However, the mechanisms through which it induces these effects are unknown. CPF has been reported to produce basal forebrain cholinergic neuronal cell death, involved on learning and memory regulation, which could be the cause of such cognitive disorders. Neuronal cell death was partially mediated by oxidative stress generation, P75 NTR and α 7 -nAChRs gene expression alteration triggered through acetylcholinesterase (AChE) variants disruption, suggesting other mechanisms are involved. In this regard, CPF induces Aβ and tau proteins production and activation of GSK3β enzyme and alters glutamatergic transmission, which have been related with basal forebrain cholinergic neuronal cell death and development of cognitive disorders. According to these data, we hypothesized that CPF induces basal forebrain cholinergic neuronal cell death through induction of Aβ and tau proteins production, activation of GSK-3β enzyme and disruption of glutamatergic transmission. We evaluated this hypothesis in septal SN56 basal forebrain cholinergic neurons, after 24 h and 14 days CPF exposure. This study shows that CPF increases glutamate levels, upregulates GSK-3β gene expression, and increases the production of Aβ and phosphorylated tau proteins and all these effects reduced cell viability. CPF increases glutaminase activity and upregulates the VGLUT1 gene expression, which could mediate the disruption of glutamatergic transmission. Our present results provide new understanding of the mechanisms contributing to the harmful effects of CPF, and its possible relevance in the pathogenesis of neurodegenerative diseases.
(Copyright © 2018 Elsevier B.V. All rights reserved.)

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