Evidence map›Paper›PMID 21868749›Full record

ArticleJournal of andrology

Induction and persistence of abnormal testicular germ cells following gestational exposure to di-(n-butyl) phthalate in p53-null mice.

Camelia M Saffarini, Nicholas E Heger, Hideki Yamasaki, Tao Liu, Susan J Hall, Kim Boekelheide

Open access · bronzeAbstract read
In one paragraph

Article in Journal of andrology. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed, 1 pooled it
1.7field-weighted citation impact, top 18% 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

16 citing papers in PubMed, 1 synthesis or guideline pooled it, 38 citations in OpenAlex.

  1. Pooled it
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  3. Article
  4. Review
  5. Review
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  7. Article
  8. Review
  9. From the Cover: Teratogenic Effects of in Utero Exposure to Di-(2-Ethylhexyl)-Phthalate (DEHP) in B6:129S4 Mice.Toxicological sciences : an official journal of the Society of Toxicology · 2017
    Article
  10. Article
  11. Article
  12. Article
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  15. Of mice and men (and rats): phthalate-induced fetal testis endocrine disruption is species-dependent.Toxicological sciences : an official journal of the Society of Toxicology · 2012
    Review
  16. 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

6 authors at 1 institution in 1 country.

Camelia M SaffariniDepartment of Pathology and Laboratory Medicine and the Center for Statistical Sciences, Brown University, Providence, RI, USA.
Nicholas E Heger
Hideki Yamasaki
Tao Liu
Susan J Hall
Kim Boekelheide
Brown University · US

Funding

TRAINING IN ENVIRONMENTAL PATHOLOGYT32ES007272 · NIEHS · BROWN UNIVERSITY · PI ZHITKOVICH, ANATOLY · 1992 to 2021
$7.5M
Molecular Mechanism of Human Fetal Testis Susceptibility to Endocrine DisruptionR01ES017272 · NIEHS · BROWN UNIVERSITY · PI BOEKELHEIDE, KIM · 2010 to 2014
$2.7M
PHTHALATE-INDUCED MURINE TESTICULAR DYSGENESIS AND P53R21ES013020 · NIEHS · BROWN UNIVERSITY · PI BOEKELHEIDE, KIM · 2005 to 2007
$453k
NIEHS NIH HHS R01 ES017272NIEHS NIH HHS R21 ES013020NIEHS NIH HHS R21ES013020NIEHS NIH HHS T32 ES007272NIEHS NIH HHS T32-ES7272
6 · The paper itself

Abstract

Phthalate esters are commonly used plasticizers found in many household items, personal care products, and medical devices. Animal studies have shown that in utero exposure to di-(n-butyl) phthalate (DBP) within a critical window during gestation causes male reproductive tract abnormalities resembling testicular dysgenesis syndrome. Our studies utilized p53-deficient mice for their ability to display greater resistance to apoptosis during development. This model was chosen to determine whether multinucleated germ cells (MNG) induced by gestational DBP exposure could survive postnatally and evolve into testicular germ cell cancer. Pregnant dams were exposed to DBP (500 mg/kg/day) by oral gavage from gestational day 12 until birth. Perinatal effects were assessed on gestational day 19 and postnatal days 1, 4, 7, and 10 for the number of MNGs present in control and DBP-treated p53-heterozygous and null animals. As expected, DBP exposure induced MNGs, with greater numbers found in p53-null mice. Additionally, there was a time-dependent decrease in the incidence of MNGs during the early postnatal period. Histologic examination of adult mice exposed in utero to DBP revealed persistence of abnormal germ cells only in DBP-treated p53-null mice, not in p53-heterozygous or wild-type mice. Immunohistochemical staining of perinatal MNGs and adult abnormal germ cells was negative for both octamer-binding protein 3/4 and placental alkaline phosphatase. This unique model identified a role for p53 in the perinatal apoptosis of DBP-induced MNGs and provided insight into the long-term effects of gestational DBP exposure within a p53-null environment.

Indexed as

Alkaline PhosphataseAnimalsApoptosisDibutyl PhthalateFemaleGonadal DysgenesisGPI-Linked ProteinsIsoenzymesMaleMiceMice, Mutant StrainsOctamer Transcription Factor-3PlasticizersPregnancyPrenatal Exposure Delayed EffectsSpermatozoaAlkaline Phosphatasealkaline phosphatase, placentalDibutyl PhthalateGPI-Linked ProteinsIsoenzymesOctamer Transcription Factor-3PlasticizersTumor Suppressor Protein p53

Identifiers

PMID21868749
PMCPMC3607946
OpenAlexW2009363672

What OpenQuestion holds

Textmetadata
LicenceTDM
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.