Evidence map›Paper›PMID 32194376›Full record

ArticleFrontiers in cellular neuroscience2020

Early Neurotoxic Effects of Inorganic Arsenic Modulate Cortical GSH Levels Associated With the Activation of the Nrf2 and NFκB Pathways, Expression of Amino Acid Transporters and NMDA Receptors and the Production of Hydrogen Sulfide.

Daniela Silva-Adaya, Lucio Antonio Ramos-Chávez, Pavel Petrosyan, Wendy Leslie González-Alfonso, Alegna Pérez-Acosta, Maria E Gonsebatt

Open access · goldAbstract read
In one paragraph

Article in Frontiers in cellular neuroscience, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
2.5field-weighted citation impact, top 12% 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

14 citing papers in PubMed, 28 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Hydrogen Sulfide (HCurrent neuropharmacology · 2022
    Review
  12. Review
  13. Article
  14. Article
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

6 authors at 3 institutions in 1 country.

Daniela Silva-AdayaDepartamento de Medicina Genómica, Instituto de Investigaciones Biomédicas, Universidad Nacional Autónoma de México, México, Mexico.
Lucio Antonio Ramos-ChávezDepartamento de Neuroquímica, Subdirección de Investigaciones Clínicas, Instituto Nacional de Psiquiatría Ramón de la Fuente, Ciudad de México, México, Mexico.
Pavel PetrosyanDepartamento de Medicina Genómica, Instituto de Investigaciones Biomédicas, Universidad Nacional Autónoma de México, México, Mexico.
Wendy Leslie González-AlfonsoDepartamento de Medicina Genómica, Instituto de Investigaciones Biomédicas, Universidad Nacional Autónoma de México, México, Mexico.
Alegna Pérez-AcostaDepartamento de Medicina Genómica, Instituto de Investigaciones Biomédicas, Universidad Nacional Autónoma de México, México, Mexico.
Maria E GonsebattDepartamento de Medicina Genómica, Instituto de Investigaciones Biomédicas, Universidad Nacional Autónoma de México, México, Mexico.
Universidad Nacional Autónoma de México · MXInstituto Nacional de Neurología y Neurocirugía · MXInstituto Nacional de Psiquiatría · MX

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Exposure to toxic metals and metalloids is an important cause of preventable diseases worldwide. Inorganic arsenic (iAs) affects several organs and tissues, causing neurobehavioral alterations in the central nervous system (CNS) that might lead to neurodegeneration. In this work, we wanted to explore the time- and dose-related changes on glutathione (GSH) levels in several regions of the CNS, such as the cortex, striatum, hippocampus, and cerebellum, to identify the initial cellular changes associated to GSH depletion due to iAs exposure. Mice received a single intraperitoneal injection containing 5 or 14 mg/kg sodium arsenite. Animals were killed at 2, 6, and 24 h. Significant depletion of GSH levels was observed in the cortex at 2 and 6 h, while on the striatum, hippocampus, or cerebellum regions, no significant changes were observed. GSH depletion in the cortex was associated with the activation of the nuclear factor erythroid 2-related factor 2 (Nrf2) and nuclear factor kappa B (NFκB) pathways, which led to the upregulation of xCT, excitatory amino acid carrier 1 (EAAC1), glutamate/aspartate transporter (GLAST), and glial glutamate transporter 1 (GLT-1), and the activation of the transsulfuration pathways, which led to the overproduction of H

Indexed as

arsenicCNS cysteine/glutamate transportersGSHH2SNFκBNrf2

Identifiers

PMID32194376
PMCPMC7065714
OpenAlexW3007259341

What OpenQuestion holds

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Registered trials

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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.