Evidence map›Paper›PMID 31652106›Full record

ArticleEnvironmental health perspectives2019

Environmentally Relevant Perinatal Exposures to Bisphenol A Disrupt Postnatal Kiss1/NKB Neuronal Maturation and Puberty Onset in Female Mice.

Francisco Ruiz-Pino, Desiree Miceli, Delphine Franssen, Maria Jesus Vazquez, Alice Farinetti, Juan Manuel Castellano, GianCarlo Panzica, Manuel Tena-Sempere

Open access · diamondAbstract read
In one paragraph

Article in Environmental health perspectives, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
3.9field-weighted citation impact, top 6% 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

20 citing papers in PubMed, 53 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. EndoCompass Project: Environmental Endocrinology.Hormone research in paediatrics · 2025
    Review
  5. Article
  6. Article
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  19. Article
  20. THE EFFECTS OF ENDOCRINE DISRUPTORS ON FEMALE GONADAL AXIS: AN UPDATE.Acta endocrinologica (Bucharest, Romania : 2005)
    Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 2 institutions in 2 countries.

Francisco Ruiz-PinoInstituto Maimónides de Investigación Biomédica de Cordoba (IMIBIC), Department of Cell Biology, Physiology and Immunology, University of Cordoba, Avda, Cordoba, Spain.
Desiree MiceliDepartment of Neuroscience "Rita Levi Montalcini," University of Torino, Torino, Italy.
Delphine FranssenInstituto Maimónides de Investigación Biomédica de Cordoba (IMIBIC), Department of Cell Biology, Physiology and Immunology, University of Cordoba, Avda, Cordoba, Spain.
Maria Jesus VazquezInstituto Maimónides de Investigación Biomédica de Cordoba (IMIBIC), Department of Cell Biology, Physiology and Immunology, University of Cordoba, Avda, Cordoba, Spain.
Alice FarinettiDepartment of Neuroscience "Rita Levi Montalcini," University of Torino, Torino, Italy.
Juan Manuel CastellanoInstituto Maimónides de Investigación Biomédica de Cordoba (IMIBIC), Department of Cell Biology, Physiology and Immunology, University of Cordoba, Avda, Cordoba, Spain.
GianCarlo PanzicaDepartment of Neuroscience "Rita Levi Montalcini," University of Torino, Torino, Italy.
Manuel Tena-SempereInstituto Maimónides de Investigación Biomédica de Cordoba (IMIBIC), Department of Cell Biology, Physiology and Immunology, University of Cordoba, Avda, Cordoba, Spain.
Instituto de Salud Carlos III · ESNeuroscience Institute · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe timing of puberty is highly sensitive to environmental factors, including endocrine disruptors. Among them, bisphenol A (BPA) has been previously analyzed as potential modifier of puberty. Yet, disparate results have been reported, with BPA advancing, delaying, or being neutral in its effects on puberty onset. Likewise, mechanistic analyses addressing the central and peripheral actions/targets of BPA at puberty remain incomplete and conflictive.

objectiveWe aimed to provide a comprehensive characterization of the impact of early BPA exposures, especially at low, real-life doses, on the postnatal development of hypothalamic Kiss1/NKB neurons, and its functional consequences on female pubertal maturation.

methodsPregnant CD1 female mice were orally administered BPA at 5, 10, or

resultsPerinatal exposure to BPA, in a range of doses largely below the no observed adverse effect level (NOAEL;

conclusionsOur data attest to the consistent, but divergent, effects of gestational exposures to low concentrations of BPA, via the oral route, on phenotypic and neuroendocrine markers of puberty in female mice, with an unambiguous impact on the developmental maturation not only of Kiss1, but also of the NKB system, both essential regulators of puberty onset. https://doi.org/10.1289/EHP5570.

Indexed as

AnimalsBenzhydryl CompoundsBisphenol A CompoundsEndocrine DisruptorsEnvironmental PollutantsFemaleKisspeptinsMiceNeuronsPhenolsPregnancyPrenatal Exposure Delayed EffectsSexual MaturationBenzhydryl Compoundsbisphenol ABisphenol A CompoundsEndocrine DisruptorsEnvironmental PollutantsKiss1 protein, mouseKisspeptinsPhenols

Identifiers

PMID31652106
PMCPMC6867420
OpenAlexW2981440694

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.