Document
type: Class

Continuant
type: Class

Entity
type: Class

Review
type: Class

Generically Dependent Continuant
type: Class

individual
rights: termsOfUse
date: 2026-08-26T23:50:46
publisher: vivo
type: Document
label: RDF description of Toxicity mechanisms of arsenic that are shared with neurodegenerative diseases and cognitive impairment: Role of oxidative stress and inflammatory responses - http://orbis.uaslp.mx/vivo/individual/scopus7070

Article
type: Class

NeuroToxicology
type: Continuant
type: Journal
type: Periodical
type: Generically Dependent Continuant
type: Document
publication venue for: Toxicity mechanisms of arsenic that are shared with neurodegenerative diseases and cognitive impairment: Role of oxidative stress and inflammatory responses
type: Information Content Entity
type: Entity
type: Collection
type: Thing

Information Content Entity
type: Class

Toxicity mechanisms of arsenic that are shared with neurodegenerative diseases and cognitive impairment: Role of oxidative stress and inflammatory responses
type: Document
most specific type: Document
most specific type: Review
type: Entity
volume: 53
type: Continuant
page end: 235
estado: published
type: Thing
related by: authorship_45765
type: Generically Dependent Continuant
chemicalscas: arsenic, 7440-38-2; Arsenic
type: Review
origen: scopus
freetext keyword: Arsenic; Inflammation; Neurodegeneration; Oxidative stress arsenic; neurotransmitter; arsenic; autophagy; bioaccumulation; biosynthesis; brain tissue; cell activation; cognitive defect; degenerative disease; disease association; disorders of mitochondrial functions; encephalitis; endoplasmic reticulum stress; environmental exposure; evidence based medicine; human; invertebrate; learning disorder; memory disorder; molecular pathology; neurotoxicity; nonhuman; oxidative stress; pathophysiology; population research; priority journal; protein aggregation; protein defect; protein degradation; protein folding; protein localization; Review; risk factor; synaptic transmission; animal; arsenic poisoning; chemically induced; cognitive defect; complication; degenerative disease; drug effects; oxidative stress; Animals; Arsenic; Arsenic Poisoning; Cognition Disorders; Humans; Neurodegenerative Diseases; Oxidative Stress
e iscopus: 2-s2.0-84958250893
page start: 223
type: Article
abstract: Arsenic (As) is a worldwide naturally occurring metalloid. Human chronic exposure to inorganic As compounds (iAs), which are at the top of hazardous substances (ATSDR, 2013), is associated with different diseases including cancer and non- cancerous diseases. The neurotoxic effects of iAs and its methylated metabolites have been demonstrated in exposed populations and experimental models. Impaired cognitive abilities have been described in children and adults chronically exposed to iAs through drinking water. Even though different association studies failed to demonstrate that As causes neurodegenerative diseases, several toxicity mechanisms of iAs parallel those mechanisms associated with neurodegeneration, including oxidative stress and inflammation, impaired protein degradation, autophagy, and intracellular accumulation, endoplasmic reticulum stress, and mitochondrial dysfunction. Additionally, different reports have shown that specifically in brain tissue, iAs and its metabolites induce hyper-phosphorylation of the tau protein and over-regulation of the amyloid precursor protein, impaired neurotransmitters synthesis and synaptic transmission, increased glutamate receptors activation, and decreased glutamate transporters expression. Interestingly, increased and sustained pro-inflammatory responses mediated by cytokines and related factors, seems to be the triggering factor for all of such cellular pathological effects. Therefore, this review proposes that iAs-associated cognitive impairment could be the result of the activation of pro-inflammatory responses in the brain tissue, which also may favor neurodegeneration or increase the risk for neurodegenerative diseases in exposed human populations. © 2016 Elsevier Inc.
type: Information Content Entity
pmid: 26868456
crisid: 7071
date time value: review date 7071
has publication venue: NeuroToxicology
doi: 10.1016/j.neuro.2016.02.002