Evidence map›Paper›PMID 26855884›Full record

ArticleToxicology reports2015

Sex-Dependent effects of developmental arsenic exposure on methylation capacity and methylation regulation of the glucocorticoid receptor system in the embryonic mouse brain.

Andrea M Allan, Alexander K Hafez, Matthew T Labrecque, Elizabeth R Solomon, M Nabil Shaikh, Xianyun Zheng, Abdulmehdi Ali

Open access · goldAbstract read
In one paragraph

Article in Toxicology reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.4field-weighted citation impact, top 19% 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

20 citing papers in PubMed, 33 citations in OpenAlex.

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  12. Prenatal metal mixtures and sex-specific infant negative affectivity.Environmental epidemiology (Philadelphia, Pa.) · 2021
    Article
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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

7 authors at 1 institution in 1 country.

Andrea M AllanDepartment of Neurosciences, University of New Mexico Health Sciences Center, Albuquerque, NM 87131, USA.
Alexander K HafezDepartment of Neurosciences, University of New Mexico Health Sciences Center, Albuquerque, NM 87131, USA.
Matthew T LabrecqueDepartment of Neurosciences, University of New Mexico Health Sciences Center, Albuquerque, NM 87131, USA.
Elizabeth R SolomonDepartment of Neurosciences, University of New Mexico Health Sciences Center, Albuquerque, NM 87131, USA.
M Nabil ShaikhDepartment of Civil Engineering, University of New Mexico, Albuquerque, NM 87131, USA.
Xianyun ZhengDepartment of Neurosciences, University of New Mexico Health Sciences Center, Albuquerque, NM 87131, USA.
Abdulmehdi AliDepartment of Earth and Planetary Sciences, University of New Mexico, Albuquerque, NM 87131, USA.
University of New Mexico · US

Funding

Prenatal arsenic exposure alters transcriptional, post-transcriptional and post-translational programming of the glucocorticoid system in a sexually dimorphic mannerR01ES019583 · NIEHS · UNIVERSITY OF NEW MEXICO HEALTH SCIS CTR · PI ALLAN, ANDREA M · 2011 to 2021
$3.3M
NIEHS NIH HHS R01 ES019583
6 · The paper itself

Abstract

Previously we have shown that prenatal moderate arsenic exposure (50 ppb) disrupts glucocorticoid receptor (GR) programming and that these changes continue into adolescence in males. However, it was not clear what the molecular mechanisms were promoting these GR programming changes or if these changes occurred in arsenic-exposed females. In the present studies, we assessed the effects of arsenic on protein and mRNA of the glucocorticoid receptor (GR) and 11β-hydroxysteroid dehydrogenase (Hsd) isozymes and compared the levels of methylation within the promoters of the Nr3c1 and Hsd11b1 genes in female fetal brain at embryonic days (E) 14 and 18. Prenatal arsenate exposure produced sex specific effects on the glucocorticoid system. Compared to males, females were resistant to arsenic induced changes in GR, 11β-Hsd-1 and 11β-Hsd-2 protein levels despite observed elevations in Nr3c1 and Hsd11b2 mRNA. This sex-specific effect was not due to differences in the methylation of the GR promoter as methylation of the Nr3c1 gene was either unchanged (region containing the egr-1 binding site) or similarly reduced (region containing the SP-1 transcription factor binding site) in both males and females exposed to arsenic. Arsenic did produce sex and age-specific changes in the methylation of Hsd11b1 gene, producing increased methylation in females at E14 and decreased methylation at E18. These changes were not attributed to changes in DNMT levels. Since arsenate metabolism could interfere with the generation of methyl donor groups, we assessed glutathione (GSH), s-adenosylmethionine (SAM) and As 3 methyltransferase (As3MT). Exposed males and females had similar levels of As3MT and SAM; however, females had higher levels of GSH/GSSH. It is possible that this greater anti-oxidative capacity within the females provides protection against low to moderate arsenate. Our data suggest that the GR signaling system in female offspring was not as affected by prenatal arsenic and predicts that female arsenic-exposed mice should have normal GR feedback regulation.

Indexed as

11B-hydroxysteroidArsenatedehydrogenase-1DNA methylationglucocorticoidglutathioneprenatalS-adenosylmethionine

Identifiers

PMID26855884
PMCPMC4741109
OpenAlexW2181914186

What OpenQuestion holds

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LicenceCC BY-NC-ND
Read underepoch 390

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.