Evidence map›Paper›PMID 22960421›Full record

ArticleNeurotoxicology2012

Perinatal exposure to 50 ppb sodium arsenate induces hypothalamic-pituitary-adrenal axis dysregulation in male C57BL/6 mice.

Samantha L Goggin, Matthew T Labrecque, Andrea M Allan

Abstract read
In one paragraph

Article in Neurotoxicology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.9field-weighted citation impact, top 15% 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

19 citing papers in PubMed, 52 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

3 authors at 1 institution in 1 country.

Samantha L GogginDepartment of Neuroscience, University of New Mexico School of Medicine, Albuquerque, NM 87131, USA.
Matthew T Labrecque
Andrea M Allan
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 1R01ES019583-01NIEHS NIH HHS R01 ES019583
6 · The paper itself

Abstract

Over the past two decades, key advancements have been made in understanding the complex pathology that occurs following not only high levels of arsenic exposure (>1 ppm) but also levels previously considered to be low (<100 ppb). Past studies have characterized the deleterious effects of arsenic on the various functions of cardiovascular, pulmonary, immunological, respiratory, endocrine and neurological systems. Other research has demonstrated an elevated risk of a multitude of cancers and increased rates of psychopathology, even at very low levels of arsenic exposure. The hypothalamic-pituitary-adrenal (HPA) axis represents a multisite integration center that regulates a wide scope of biological and physiological processes: breakdown within this system can generate an array of far-reaching effects, making it an intriguing candidate for arsenic-mediated damage. Using a mouse model, we examined the effects of perinatal exposure to 50 ppb sodium arsenate on the functioning of the HPA axis through the assessment of corticotrophin-releasing factor (CRF), proopiomelanocortin (Pomc) mRNA, adrenocorticotrophin hormone (ACTH), corticosterone (CORT), 11β-hydroxysteroid dehydrogenase Type 1 (11β-HSD 1), and glucocorticoid receptor (GR) protein and mRNA. Compared to controls, we observed that the perinatal arsenic-exposed offspring exhibit an increase in hypothalamic CRF, altered CORT secretion both at baseline and in response to a stressor, decreased hippocampal 11β-HSD 1 and altered subcellular GR distribution in the hypothalamus. These data indicate significant HPA axis impairment at post-natal day 35 resulting from perinatal exposure to 50 ppb sodium arsenate. Our findings suggest that the dysregulation of this critical regulatory axis could underlie important molecular and cognitive pathology observed following exposure to arsenic.

Indexed as

11-beta-Hydroxysteroid Dehydrogenase Type 1Adrenocorticotropic HormoneAnalysis of VarianceAnimalsAnimals, NewbornArsenatesEnzyme-Linked Immunosorbent AssayFeeding BehaviorHypothalamo-Hypophyseal SystemHypoxanthine PhosphoribosyltransferaseMaleMiceMice, Inbred C57BLPituitary-Adrenal SystemReceptors, GlucocorticoidRNA, Messenger11-beta-Hydroxysteroid Dehydrogenase Type 1Adrenocorticotropic HormoneArsenatesHypoxanthine PhosphoribosyltransferaseReceptors, GlucocorticoidRNA, Messengersodium arsenateWater Pollutants

Identifiers

PMID22960421
PMCPMC3470737
OpenAlexW2110540914

What OpenQuestion holds

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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.