Evidence map›Paper›PMID 30675821›Full record

ArticleEnvironmental health perspectives2018

Use of a Mouse Model of Experimentally Induced Endometriosis to Evaluate and Compare the Effects of Bisphenol A and Bisphenol AF Exposure.

Rebecca L Jones, Stephanie A Lang, Jessica A Kendziorski, Alexis D Greene, Katherine A Burns

Open access · diamondAbstract read
In one paragraph

Article in Environmental health perspectives, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed, 2 pooled it
7.7field-weighted citation impact, top 2% 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

30 citing papers in PubMed, 2 syntheses or guidelines pooled it, 85 citations in OpenAlex.

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  17. Bisphenol S Increases Cell Number and Stimulates Migration of Endometrial Epithelial Cells.Journal of the ASEAN Federation of Endocrine Societies · 2023
    Article
  18. Review
  19. Article
  20. The impact of bisphenol A on the placenta†.Biology of reproduction · 2022
    Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

5 authors at 2 institutions in 1 country.

Rebecca L JonesDepartment of Environmental Health, University of Cincinnati College of Medicine, Cincinnati, Ohio, USA.
Stephanie A LangDepartment of Environmental Health, University of Cincinnati College of Medicine, Cincinnati, Ohio, USA.
Jessica A KendziorskiDepartment of Environmental Health, University of Cincinnati College of Medicine, Cincinnati, Ohio, USA.
Alexis D GreeneDepartment of Obstetrics and Gynecology, University of Cincinnati Center for Reproductive Health, Cincinnati, Ohio, USA.
Katherine A BurnsDepartment of Environmental Health, University of Cincinnati College of Medicine, Cincinnati, Ohio, USA.
University of Cincinnati Medical Center · USInstitute for Reproductive Health · US

Funding

Endometriosis and Environmental Endocrine Disrupting Chemical ExposureR00ES021737 · NIEHS · UNIVERSITY OF CINCINNATI · PI BURNS, KATHERINE ANNE · 2015 to 2017
$737k
NIEHS NIH HHS R00 ES021737
6 · The paper itself

Abstract

backgroundEndometriosis is a gynecological disease affecting 1 in 10 women of reproductive age. Endometriosis incidence has risen; however, whether this rise is due to disease awareness or environmental contamination is not known.

objectiveThe objective of this study was to determine if bisphenol A (BPA) or bisphenol AF (BPAF) potentiate the development of endometriosis and if hormonal status alters how toxicant exposure affects disease.

methodsA mouse model of endometriosis, where minced uterine tissue is injected into the peritoneal cavity of a host mouse, was used to examine the effects of BPA and BPAF on endometriosis lesion development in ovariectomized and hormonally intact mice. BPA and BPAF were delivered through diet to include no-observed-adverse-effect-level (NOAEL) and the low-observed-adverse-effect-level (LOAEL) exposure levels. After six weeks (at necropsy), lesions, ovaries, and blood were collected to examine characteristics, gene expression, and hormonal regulation.

resultsBPA and BPAF treatments affected endometriosis in a manner specific to dose and hormonal status of the host mouse. Estrogen and endometriosis-mediated differences in lesion target gene expression also depended on hormonal status. In intact mice, ovarian steroidogenic pathways were disrupted, progesterone levels were lowered, and atretic oocyte numbers were higher with toxicant exposure. BPAF, more so than BPA, resulted in more endometriosis lesion growth, but both toxicants disrupted normal ovarian signaling.

conclusionThese findings further our understanding of the effects and hormonal impacts of BPA and BPAF on endometriosis perturbation in ovariectomized and hormonally intact mice. BPAF appeared to be similar if not more estrogenic than BPA and may be affecting an environmental contribution of the increased incidence of endometriosis. https://doi.org/10.1289/EHP3802.

Indexed as

AnimalsBenzhydryl CompoundsBisphenol A CompoundsEndocrine DisruptorsEndometriosisEstrogensFemaleFluorocarbonsGene ExpressionMice, Inbred C57BLMice, TransgenicModels, AnimalOocytesOvariectomyOvaryPhenolsBenzhydryl Compoundsbisphenol ABisphenol A Compoundsbisphenol AFEndocrine DisruptorsEstrogensFluorocarbonsPhenolsProgesterone

Identifiers

PMID30675821
PMCPMC6371646
OpenAlexW2904543591

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.