Evidence map›Paper›PMID 24804967›Full record

ArticleBiology of reproduction2014

Daily exposure to Di(2-ethylhexyl) phthalate alters estrous cyclicity and accelerates primordial follicle recruitment potentially via dysregulation of the phosphatidylinositol 3-kinase signaling pathway in adult mice.

Patrick R Hannon, Jackye Peretz, Jodi A Flaws

Open access · bronzeAbstract read
In one paragraph

Article in Biology of reproduction, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 90 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
90citing papers in PubMed, 1 pooled it
9.2field-weighted citation impact, top 1% 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

90 citing papers in PubMed, 1 synthesis or guideline pooled it, 185 citations in OpenAlex.

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30 more citing papers are in PubMed but not listed here.

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.

Patrick R HannonDepartment of Comparative Biosciences, University of Illinois at Urbana-Champaign, Urbana, Illinois.
Jackye PeretzDepartment of Comparative Biosciences, University of Illinois at Urbana-Champaign, Urbana, Illinois.
Jodi A FlawsDepartment of Comparative Biosciences, University of Illinois at Urbana-Champaign, Urbana, Illinois jflaws@illinois.edu.
University of Illinois Urbana-Champaign · US

Funding

Endocrine disrupting chemicals and ovotoxicityR01ES019178 · NIEHS · UNIVERSITY OF ILLINOIS AT URBANA-CHAMPAIGN · PI FLAWS, JODI A. · 2010 to 2014
$1.9M
NIEHS NIH HHS R01 ES019178NIEHS NIH HHS R01ES019178
6 · The paper itself

Abstract

Humans are exposed daily to di(2-ethylhexyl) phthalate (DEHP), a plasticizer found in many consumer, medical, and building products containing polyvinyl chloride. Large doses of DEHP disrupt normal ovarian function; however, the effects of DEHP at environmentally relevant levels, the effects of DEHP on folliculogenesis, and the mechanisms by which DEHP disrupts ovarian function are unclear. The present study tested the hypothesis that relatively low levels of DEHP disrupt estrous cyclicity as well as accelerate primordial follicle recruitment by dysregulating phosphatidylinositol 3-kinase (PI3K) signaling. Adult CD-1 mice were orally dosed with DEHP (20 μg/kg/day-750 mg/kg/day) daily for 10 and 30 days. Following dosing, the effects on estrous cyclicity were examined, and follicle numbers were histologically quantified. Further, the ovarian mRNA and protein levels of PI3K signaling factors that are associated with early folliculogenesis were quantified. The data indicate that 10- and 30-day exposure to DEHP prolonged the duration of estrus and accelerated primordial follicle recruitment. Specifically, DEHP exposure decreased the percentage of primordial follicles and increased the percentage of primary follicles counted following 10-day exposure and increased the percentage of primary follicles counted following 30-day exposure. DEHP exposure, at doses that accelerate folliculogenesis, increased the levels of 3-phosphoinositide-dependent protein kinase-1, mammalian target of rapamycin complex 1, and protein kinase B and decreased the levels of phosphatase and tensin homolog, potentially driving PI3K signaling. Collectively, relatively low levels of DEHP disrupt estrous cyclicity and accelerate primordial follicle recruitment potentially via a mechanism involving dysregulation of PI3K signaling.

Indexed as

Age FactorsAnimalsCarrier ProteinsDiethylhexyl PhthalateDose-Response Relationship, DrugEndocrine DisruptorsEstrous CycleFemaleGene ExpressionMembrane ProteinsMice, Inbred StrainsOvarian FolliclePhosphatidylinositol 3-KinasePlasticizersSignal TransductionCarrier ProteinsDiethylhexyl PhthalateEndocrine DisruptorsMembrane ProteinsNFXL1 protein, humanPhosphatidylinositol 3-KinasePlasticizersdi(2-ethylhexyl) phthalateendocrine disruptorsenvironmental contaminants and toxicantsfollicular developmentfolliculogenesisovaryphosphatidylinositol 3-kinase signaling pathwaytoxicology

Identifiers

PMID24804967
PMCPMC4435463
OpenAlexW2120485749

What OpenQuestion holds

Textmetadata
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.