Increased Levels of Phosphorylated-P38α Induce WNT/β-Catenin and NGF/P75NTR/TrkA Pathways Disruption and SN56 Cell Death following Single and Repeated Chlorpyrifos Treatment

Chlorpyrifos (CPF) biocide, exposure to which is mainly produced in the human population through diet, induces several neurotoxic effects. CPF single and repeated exposure induces memory and learning disorders, although the mechanisms that produce these outcomes are complex and not well understood....

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Detalles Bibliográficos
Autores: Moyano-Cires Ivanoff, Paula Viviana, Flores Calle, Andrea, Fernández Fernández, María De La Cabeza, García Lobo, Jimena, Sanjuán López, Javier, Plaza Hernández, José Carlos, Pino Sans, Javier Del
Tipo de recurso: artículo
Fecha de publicación:2024
País:España
Institución:Universidad Complutense de Madrid (UCM)
Repositorio:Docta Complutense
Idioma:inglés
OAI Identifier:oai:docta.ucm.es:20.500.14352/107848
Acceso en línea:https://hdl.handle.net/20.500.14352/107848
Access Level:acceso abierto
Palabra clave:641.1
Chlorpyrifos
Basal forebrain cholinergic neurons
P38α
WNT/β-Catenin pathway
NGF/P75NTR/TrkA pathway
Toxicología (Farmacia)
Toxicología (Medicina)
Alimentación
3214 Toxicología
3206 Ciencias de la Nutrición
Descripción
Sumario:Chlorpyrifos (CPF) biocide, exposure to which is mainly produced in the human population through diet, induces several neurotoxic effects. CPF single and repeated exposure induces memory and learning disorders, although the mechanisms that produce these outcomes are complex and not well understood. CPF treatment (single and repeated) of cholinergic septal SN56 cells induced an increase in phosphorylated-P38α levels that led to WNT/β-Catenin and NGF/P75NTR/TrkA pathways disruption and cell death. These results provide new knowledge on the mechanisms that mediate CPF basal forebrain cholinergic neuronal loss induced by CPF single and repeated exposure and can help unravel the way through which this compound produces cognitive decline and develop efficient treatments against these effects.