Evidence map›Paper›PMID 26167515›Full record

ArticleEndocrine disruptors (Austin, Tex.)

Gestational bisphenol A exposure and testis development.

Cecilia Williams, Maria Bondesson, Dimitry N Krementsov, Cory Teuscher

Abstract read
In one paragraph

Article in Endocrine disruptors (Austin, Tex.). The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
–field-weighted citation impact
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

13 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Bisphenol AF and Bisphenol F Induce Similar Feminizing Effects in Chicken Embryo Testis as Bisphenol A.Toxicological sciences : an official journal of the Society of Toxicology · 2020
    Article
  7. Article
  8. Review
  9. Understanding the molecular mechanisms of bisphenol A action in spermatozoa.Clinical and experimental reproductive medicine · 2019
    Review
  10. Article
  11. Article
  12. DNA methylation and transcriptome aberrations mediated by ERα in mouse seminal vesicles following developmental DES exposure.Proceedings of the National Academy of Sciences of the United States of America · 2018
    Article
  13. Review
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.

Cecilia WilliamsCenter for Nuclear Receptors and Cell Signaling; Department of Biology and Biochemistry; University of Houston, Houston, TX USA.
Maria BondessonCenter for Nuclear Receptors and Cell Signaling; Department of Biology and Biochemistry; University of Houston, Houston, TX USA.
Dimitry N KrementsovDepartment of Medicine; Immunobiology Program; University of Vermont; Burlington, VT USA.
Cory TeuscherDepartment of Medicine; Immunobiology Program; University of Vermont; Burlington, VT USA ; Department of Pathology; University of Vermont; Burlington, VT USA.

Funding

Susceptibilty and Resistance Loci in Mouse EAER01NS036526 · NINDS · UNIVERSITY OF VERMONT &ST AGRIC COLLEGE · PI TEUSCHER, CORY · 1996 to 2008
$4.4M
H1R Signaling and Immune Deviation in EAER01NS069628 · NINDS · UNIVERSITY OF VERMONT & ST AGRIC COLLEGE · PI TEUSCHER, CORY · 2010 to 2014
$1.6M
Elucidating the mechanism of ERbeta in colon carcinogenesisR01CA172437 · NCI · UNIVERSITY OF HOUSTON · PI WILLIAMS, CECILIA MARIE · 2013 to 2018
$1.4M
Sex Chromosomes in Fetal Programming and Susceptibility to EAER01NS060901 · NINDS · UNIVERSITY OF VERMONT & ST AGRIC COLLEGE · PI TEUSCHER, CORY · 2008 to 2010
$1.4M
p38 MAPK as a female-specific druggable target in CNS autoimmune diseaseR21NS076200 · NINDS · UNIVERSITY OF VERMONT & ST AGRIC COLLEGE · PI TEUSCHER, CORY · 2011 to 2012
$419k
Detection of Obesogens and Diabetogens by Zebrafish Screening ModelsR21ES020036 · NIEHS · UNIVERSITY OF HOUSTON · PI GUSTAFSSON, JAN-AKE · 2012 to 2013
$371k
NCI NIH HHS R01 CA172437NIEHS NIH HHS R21 ES020036NINDS NIH HHS R01 NS036526NINDS NIH HHS R01 NS060901NINDS NIH HHS R01 NS069628NINDS NIH HHS R21 NS076200
6 · The paper itself

Abstract

Virtually all humans are exposed to bisphenol A (BPA). Since BPA can act as a ligand for estrogen receptors, potential hazardous effects of BPA should be evaluated in the context of endogenous estrogenic hormones. Because estrogen is metabolized in the placenta, developing fetuses are normally exposed to very low endogenous estrogen levels. BPA, on the other hand, passes through the placenta and might have distinct adverse consequences during the sensitive stages of fetal development. Testicular gametogenesis and steroidogenesis begin early during fetal development. These processes are sensitive to estrogens and play a role in determining the number of germ stem cells, sperm count, and male hormone levels in adulthood. Although studies have shown a correlation between BPA exposure and perturbed reproduction, a clear consensus has yet to be established as to whether current human gestational BPA exposure results in direct adverse effects on male genital development and reproduction. However, studies in animals and in vitro have provided direct evidence for the ability of BPA exposure to influence male reproductive development. This review discusses the current knowledge of potential effects of BPA exposure on male reproductive health and whether gestational exposure adversely affects testis development.

Indexed as

bisphenol Aestrogen receptorsreproductive toxicologytestis development

Identifiers

PMID26167515
PMCPMC4495970

What OpenQuestion holds

Textmetadata
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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.