Evidence map›Paper›PMID 19535786›Full record

ArticleBiology of reproduction2009

Neonatal bisphenol-a exposure alters rat reproductive development and ovarian morphology without impairing activation of gonadotropin-releasing hormone neurons.

Heather B Adewale, Wendy N Jefferson, Retha R Newbold, Heather B Patisaul

Open access · bronzeAbstract read
In one paragraph

Article in Biology of reproduction, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
75citing papers in PubMed, 2 pooled it
10.8field-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

75 citing papers in PubMed, 2 syntheses or guidelines pooled it, 200 citations in OpenAlex.

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  20. Bisphenol A: an emerging threat to female fertility.Reproductive biology and endocrinology : RB&E · 2020
    Review

15 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

4 authors at 2 institutions in 1 country.

Heather B AdewaleDepartment of Biology, North Carolina State University, Raleigh, North Carolina, USA.
Wendy N Jefferson
Retha R Newbold
Heather B Patisaul
National Institute of Environmental Health Sciences · USNorth Carolina State University · US

Funding

Endocrine Disruption of the Hypothalamic Signaling That Regulates PubertyR01ES016001 · NIEHS · NORTH CAROLINA STATE UNIVERSITY RALEIGH · PI PATISAUL, HEATHER B · 2007 to 2011
$2.0M
DEVELOPMENTAL BIOLOGY/TOXICOLOGY OF ESTROGENIC ENVIRONMENTAL CHEMICALSZ01ES070060 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI NEWBOLD, RETHA R · 1985 to 2008
$607k
Developmental Biology/Toxicology Of Estrogenic Environmental ChemicalsZIAES070060 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI NEWBOLD, RETHA R · 2009 to 2009
$164k
NIEHS NIH HHS R01 ES016001
6 · The paper itself

Abstract

Developmental exposure to endocrine-disrupting compounds is hypothesized to adversely affect female reproductive physiology by interfering with the organization of the hypothalamic-pituitary-gonadal axis. Here, we compared the effects of neonatal exposure to two environmentally relevant doses of the plastics component bisphenol-A (BPA; 50 microg/kg and 50 mg/kg) with the ESR1 (formerly known as ERalpha)-selective agonist 4,4',4''-(4-propyl-[(1)H]pyrazole-1,3,5-triyl)trisphenol (PPT; 1 mg/kg) on the development of the female rat hypothalamus and ovary. An oil vehicle and estradiol benzoate (EB; 25 microg) were used as negative and positive controls. Exposure to EB, PPT, or the low dose of BPA advanced pubertal onset. A total of 67% of females exposed to the high BPA dose were acyclic by 15 wk after vaginal opening compared with 14% of those exposed to the low BPA dose, all of the EB- and PPT-treated females, and none of the control animals. Ovaries from the EB-treated females were undersized and showed no evidence of folliculogenesis, whereas ovaries from the PPT-treated females were characterized by large antral-like follicles, which did not appear to support ovulation. Severity of deficits within the BPA-treated groups increased with dose and included large antral-like follicles and lower numbers of corpora lutea. Sexual receptivity, examined after ovariectomy and hormone replacement, was normal in all groups except those neonatally exposed to EB. FOS induction in hypothalamic gonadotropic (GnRH) neurons after hormone priming was impaired in the EB- and PPT-treated groups but neither of the BPA-treated groups. Our data suggest that BPA disrupts ovarian development but not the ability of GnRH neurons to respond to steroid-positive feedback.

Indexed as

AnimalsAnimals, NewbornBenzhydryl CompoundsBisphenol A CompoundsDose-Response Relationship, DrugEstrogens, Non-SteroidalEstrous CycleFemaleGonadotropin-Releasing HormoneHypothalamusMaleNeuroendocrine CellsOvaryPhenolsProto-Oncogene Proteins c-fosRatsBenzhydryl Compoundsbisphenol ABisphenol A CompoundsEstrogens, Non-SteroidalGonadotropin-Releasing HormonePhenolsProto-Oncogene Proteins c-fos

Identifiers

PMID19535786
PMCPMC2754884
OpenAlexW2141812339

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.