Evidence map›Paper›PMID 26863571›Full record

ArticleOncotarget2016

Neonatal bisphenol A exposure induces meiotic arrest and apoptosis of spermatogenic cells.

Meina Xie, Pengli Bu, Fengjie Li, Shijian Lan, Hongjuan Wu, Lu Yuan, Ying Wang

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
6.0field-weighted citation impact, top 4% 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

19 citing papers in PubMed, 65 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Influence of Risk Factors for Male Infertility on Sperm Protein Composition.International journal of molecular sciences · 2021
    Review
  5. Article
  6. Review
  7. Article
  8. Review
  9. Article
  10. Endocrine-disrupting chemicals and male reproductive health.Reproductive medicine and biology · 2020
    Review
  11. Article
  12. Article
  13. Neuro-toxic and Reproductive Effects of BPA.Current neuropharmacology · 2019
    Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
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

7 authors at 2 institutions in 2 countries.

Meina XieMedicine Experiment Center, Weifang Medical University, Wei Fang 261053, P. R. China.
Pengli BuDepartment of Biological Sciences, St. John's University, Queens, NY 11439, USA.
Fengjie LiMedicine Experiment Center, Weifang Medical University, Wei Fang 261053, P. R. China.
Shijian LanSchool of Bioscience and Technology, Weifang Medical University, Wei Fang 261053, P. R. China.
Hongjuan WuSchool of Basic Medical Sciences, Weifang Medical University, Wei Fang 261053, P. R. China.
Lu YuanSchool of Bioscience and Technology, Weifang Medical University, Wei Fang 261053, P. R. China.
Ying WangSchool of Bioscience and Technology, Weifang Medical University, Wei Fang 261053, P. R. China.
Weifang Medical University · CNSt. John's University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Bisphenol A (BPA) is a widely used industrial plasticizer, which is ubiquitously present in the environment and organisms. As an endocrine disruptor, BPA has caused significant concerns regarding its interference with reproductive function. However, little is known about the impact of BPA exposure on early testicular development. The aim of the present study was to investigate the influence of neonatal BPA exposure on the first wave of spermatogenesis. Newborn male mice were subcutaneously injected with BPA (0.01, 0.1 and 5 mg/kg body weight) daily from postnatal day (PND) 1 to 21. Histological analysis of testes at PND 22 revealed that BPA-treated testes contained mostly spermatogonia and spermatocytes with markedly less round spermatids, indicating signs of meiotic arrest. Terminal dUTP nick-end labeling (TUNEL) assay showed that BPA treatment significantly increased the number of apoptotic germ cells per tubule, which corroborated the observation of meiotic arrest. In addition, BPA caused abnormal proliferation of germ cells as revealed by Proliferating Cell Nuclear Antigen (PCNA) immunohistochemical staining. Mechanistically, BPA-treated testes displayed a complete lack of BOULE expression, which is a conserved key regulator for spermatogenesis. Moreover, BPA significantly increased the expression of estrogen receptor (ER) α and β in the developing testis. The present study demonstrated that neonatal BPA exposure disrupted meiosis progression during the first wave of spermatogenesis, which may be, at least in part, due to inhibition of BOULE expression and/or up-regulation of ERα/β expression in BPA-exposed developing testis.

Indexed as

AnimalsApoptosisBenzhydryl CompoundsBisphenol A CompoundsCell ProliferationEndocrine DisruptorsEstrogen Receptor alphaEstrogen Receptor betaIn Situ Nick-End LabelingMaleMeiosisMiceMice, Inbred ICRPhenolsRNA-Binding ProteinsSpermatidsBenzhydryl Compoundsbisphenol ABisphenol A CompoundsBoll protein, mouseEndocrine DisruptorsEstrogen Receptor alphaEstrogen Receptor betaPhenolsRNA-Binding Proteinsbisphenol ABouleestrogen receptor α/βmeiotic arrestspermatogenic cells

Identifiers

PMID26863571
PMCPMC4891144
OpenAlexW2288264962

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.