Evidence map›Paper›PMID 31748979›Full record

ReviewJournal of biological inorganic chemistry : JBIC : a publication of the Society of Biological Inorganic Chemistry2019

Arsenic-induced neurotoxicity: a mechanistic appraisal.

Carla Garza-Lombó, Aglaia Pappa, Mihalis I Panayiotidis, María E Gonsebatt, Rodrigo Franco

Open access · greenAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Journal of biological inorganic chemistry : JBIC : a publication of the Society of Biological Inorganic Chemistry, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
6.9field-weighted citation impact, top 2% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

45 citing papers in PubMed, 160 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 4 institutions in 4 countries.

Carla Garza-LombóRedox Biology Center, University of Nebraska-Lincoln, Lincoln, NE, 68588, USA.
Aglaia PappaDepartment of Molecular Biology and Genetics, Democritus University of Thrace, Alexandroupolis, Greece.
Mihalis I PanayiotidisDepartment of Applied Sciences, Northumbria University, Newcastle upon Tyne, UK.
María E GonsebattDepartamento de Medicina Genómica y Toxicología Ambiental, Instituto de Investigaciones Biomédicas, Universidad Nacional Autónoma de México, 04510, Mexico City, Mexico.
Rodrigo FrancoRedox Biology Center, University of Nebraska-Lincoln, Lincoln, NE, 68588, USA. rfrancocruz2@unl.edu.
University of Nebraska–Lincoln · USDemocritus University of Thrace · GRNorthumbria University · GBUniversidad Nacional Autónoma de México · MX

Funding

THE REDOX-MEDIATED REGULATION OF IRON-RESPONSIVE GENE EXPRESSION IN LIVERP20RR017675 · NCRR · UNIVERSITY OF NEBRASKA LINCOLN · PI BECKER, DONALD F · 2002 to 2011
$20.4M
Redox Biology CenterP30GM103335 · NIGMS · UNIVERSITY OF NEBRASKA LINCOLN · PI BECKER, DONALD F · 2012 to 2016
$4.3M
NCRR NIH HHS P20 RR017675NIGMS NIH HHS P30 GM103335NIH Clinical Center P20RR17675
6 · The paper itself

Abstract

Arsenic is a metalloid found in groundwater as a byproduct of soil/rock erosion and industrial and agricultural processes. This xenobiotic elicits its toxicity through different mechanisms, and it has been identified as a toxicant that affects virtually every organ or tissue in the body. In the central nervous system, exposure to arsenic can induce cognitive dysfunction. Furthermore, iAs has been linked to several neurological disorders, including neurodevelopmental alterations, and is considered a risk factor for neurodegenerative disorders. However, the exact mechanisms involved are still unclear. In this review, we aim to appraise the neurotoxic effects of arsenic and the molecular mechanisms involved. First, we discuss the epidemiological studies reporting on the effects of arsenic in intellectual and cognitive function during development as well as studies showing the correlation between arsenic exposure and altered cognition and mental health in adults. The neurotoxic effects of arsenic and the potential mechanisms associated with neurodegeneration are also reviewed including data from experimental models supporting epidemiological evidence of arsenic as a neurotoxicant. Next, we focused on recent literature regarding arsenic metabolism and the molecular mechanisms that begin to explain how arsenic damages the central nervous system including, oxidative stress, energy failure and mitochondrial dysfunction, epigenetics, alterations in neurotransmitter homeostasis and synaptic transmission, cell death pathways, and inflammation. Outlining the specific mechanisms by which arsenic alters the cell function is key to understand the neurotoxic effects that convey cognitive dysfunction, neurodevelopmental alterations, and neurodegenerative disorders.

Indexed as

AnimalsApoptosisArsenicArsenic PoisoningAutophagyEpigenesis, GeneticHippocampusHumansMitochondriaNeuronsOxidative StressArseniciAsMetalloidNeurotoxicityOxidative stressRedox homeostasis

Identifiers

PMID31748979
PMCPMC6903391
OpenAlexW2990913121

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.