Evidence map›Paper›PMID 29524743›Full record

ArticleAquatic toxicology (Amsterdam, Netherlands)2018

Nrf2a modulates the embryonic antioxidant response to perfluorooctanesulfonic acid (PFOS) in the zebrafish, Danio rerio.

Karilyn E Sant, Paul P Sinno, Haydee M Jacobs, Alicia R Timme-Laragy

Open access · greenAbstract read
In one paragraph

Article in Aquatic toxicology (Amsterdam, Netherlands), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
3.7field-weighted citation impact, top 7% 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

27 citing papers in PubMed, 60 citations in OpenAlex.

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  11. Review of the zebrafish as a model to investigate per- and polyfluoroalkyl substance toxicity.Toxicological sciences : an official journal of the Society of Toxicology · 2023
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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

4 authors at 1 institution in 1 country.

Karilyn E SantDepartment of Environmental Health Sciences, School of Public Health and Health Sciences, University of Massachusetts, Amherst, MA 01003, United States.
Paul P SinnoDepartment of Environmental Health Sciences, School of Public Health and Health Sciences, University of Massachusetts, Amherst, MA 01003, United States.
Haydee M JacobsDepartment of Environmental Health Sciences, School of Public Health and Health Sciences, University of Massachusetts, Amherst, MA 01003, United States.
Alicia R Timme-LaragyDepartment of Environmental Health Sciences, School of Public Health and Health Sciences, University of Massachusetts, Amherst, MA 01003, United States. Electronic address: aliciat@umass.edu.
University of Massachusetts Amherst · US

Funding

Activation of Nrf2 during embryonic development: mechanisms and consequencesR01ES025748 · NIEHS · UNIVERSITY OF MASSACHUSETTS AMHERST · PI Alicia R Timme-Laragy · 2016 to 2026
$4.0M
Toxicant disruption of receptor-mediated endocytosis in oogenesis and later life metabolic dysfunctionR01ES028201 · NIEHS · UNIVERSITY OF MASSACHUSETTS AMHERST · PI TIMME-LARAGY, ALICIA R · 2017 to 2021
$2.1M
Interactions between PPAR, embryonic nutrition, and the developmental origins of metabolic dysfunctionF32ES028085 · NIEHS · UNIVERSITY OF MASSACHUSETTS AMHERST · PI SANT, KARILYN ELIZABETH · 2017 to 2018
$82k
NIEHS NIH HHS F32 ES028085NIEHS NIH HHS R01 ES025748NIEHS NIH HHS R01 ES028201
6 · The paper itself

Abstract

The glutathione redox system undergoes precise and dynamic changes during embryonic development, protecting against and mitigating oxidative insults. The antioxidant response is coordinately largely by the transcription factor Nuclear factor erythroid-2 (Nrf2), an endogenous sensor for cellular oxidative stress. We have previously demonstrated that impaired Nrf family signaling disrupts the glutathione redox system in the zebrafish embryo, and that impaired Nrf2 function increases embryonic sensitivity to environmental toxicants. Here, we investigated the persistent environmental toxicant and reported pro-oxidant perfluorooctanesulfonic acid (PFOS), and its impact on the embryonic glutathione-mediated redox environment. We further examined whether impaired Nrf2a function exacerbates PFOS-induced oxidative stress and embryotoxicity in the zebrafish, and the potential for Nrf2-PPAR crosstalk in the embryonic adaptive response. Wild-type and nrf2a

Indexed as

Alkanesulfonic AcidsAntioxidantsEmbryo, NonmammalianFluorocarbonsZebrafishZebrafish ProteinsAnimalsApoptosisBinding SitesCysteineEmbryonic DevelopmentGene Expression Regulation, DevelopmentalGlutathioneNF-E2-Related Factor 2Oxidation-ReductionOxidative StressAlkanesulfonic AcidsAntioxidantsCysteineFluorocarbonsGlutathionenfe2l2a protein, zebrafishNF-E2-Related Factor 2perfluorooctane sulfonic acidPeroxisome Proliferator-Activated ReceptorsReactive Oxygen SpeciesTranscription FactorsWater Pollutants, ChemicalZebrafish ProteinsEmbryoGlutathioneNfe2l2PerfluorinatedPFASRedox

Identifiers

PMID29524743
PMCPMC6077977
OpenAlexW2793332523

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.