Mechanisms associated with cognitive and behavioral impairment induced by arsenic exposure

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dc.contributor.affiliationNeurobiochemistry and Behavior Laboratory, National Institute of Neurology and Neurosurgery “Manuel Velasco Suárez”, Mexico City 14269, Mexico
dc.contributor.emailveped@yahoo.com.mx
dc.creatorVázquez Cervantes, Gustavo Ignacioes_ES
dc.creatorGonzález Esquivel, Dinora Fabiolaes_ES
dc.creatorRamírez Ortega, Danielaes_ES
dc.creatorBlanco Ayala, Tonalies_ES
dc.creatorRamos Chávez, Lucio Antonioes_ES
dc.creatorLópez-López, Humberto Emanueles_ES
dc.creatorSalazar, Alelíes_ES
dc.creatorFlores, Itamares_ES
dc.creatorPineda, Benjamínes_ES
dc.creatorGómez-Manzo, Saúles_ES
dc.creatorPérez de la Cruz, Verónicaes_ES
dc.date2023
dc.date.accessioned2025-03-12T18:11:32Z
dc.date.accessioned2026-03-27T15:31:16Z
dc.date.available2025-03-12T18:11:32Z
dc.date.issued2023
dc.date.published2023
dc.descriptionArsenic (As) is a metalloid naturally present in the environment, in food, water, soil, and air; however, its chronic exposure, even with low doses, represents a public health concern. For a long time, As was used as a pigment, pesticide, wood preservative, and for medical applications; its industrial use has recently decreased or has been discontinued due to its toxicity. Due to its versatile applications and distribution, there is a wide spectrum of human As exposure sources, mainly contaminated drinking water. The fact that As is present in drinking water implies chronic human exposure to this metalloid; it has become a worldwide health problem, since over 200 million people live where As levels exceed safe ranges. Many health problems have been associated with As chronic exposure including cancer, cardiovascular diseases, gastrointestinal disturbances, and brain dysfunctions. Because As can cross the blood-brain barrier (BBB), the brain represents a target organ where this metalloid can exert its long-term toxic effects. Many mechanisms of As neurotoxicity have been described: oxidative stress, inflammation, DNA damage, and mitochondrial dysfunction; all of them can converge, thus leading to impaired cellular functions, cell death, and in consequence, long-term detrimental effects. Here, we provide a current overview of As toxicity and integrated the global mechanisms involved in cognitive and behavioral impairment induced by As exposure show experimental strategies against its neurotoxicity.es_ES
dc.formatPDFes_ES
dc.identifierJC06NC23es_ES
dc.identifier.doi10.3390/cells12212537
dc.identifier.eissn2073-4409
dc.identifier.organizacionInstituto Nacional de Psiquiatría Ramón de la Fuente Muñiz
dc.identifier.placeSuiza
dc.identifier.urihttps://doi.org/10.3390/cells12212537
dc.identifier.urihttps://repositorio.inprf.gob.mx/handle/123456789/8243
dc.language.isoenges_ES
dc.publisherMDPIes_ES
dc.relation12(21):2537
dc.relation.jnabreviadoCELLS
dc.relation.journalCell
dc.rightsAcceso Cerradoes_ES
dc.subject.kwNeurotoxicity
dc.subject.kwCognition
dc.subject.kwMetalloids exposure
dc.subject.kwArsenic
dc.titleMechanisms associated with cognitive and behavioral impairment induced by arsenic exposurees_ES
dc.typeArtículoes_ES

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