Document Detail


Sertoli cell development and function in an animal model of testicular dysgenesis syndrome.
MedLine Citation:
PMID:  17928633     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Pregnancy exposure to di(n-butyl) phthalate (DBP) in rats induces a testicular dysgenesislike syndrome (TDS) in male offspring. Earlier studies suggested altered Sertoli cell development/maturation may result, especially in testes that become cryptorchid. This study quantitatively assessed Sertoli cell numerical and functional development in DBP-exposed rats and compared (unilaterally) cryptorchid and scrotal testes. Pregnant rats were gavaged with 500 mg/kg/day DBP or corn oil from embryonic (E) Days 13.5 to 21.5. Male offspring were sampled on E21.5 or Postnatal Day 6, 10, 15, 25, or 90. Sertoli cell number in DBP-exposed males was reduced by approximately 50% at E21.5 but recovered to normal by Days 25-90, accompanied by significant changes in plasma inhibin B and testosterone levels. Sertoli cell maturational development in DBP-exposed males, assessed using five protein markers (anti-müllerian hormone, cytokeratin, androgen receptor, CDKN1B, and Nestin), was largely normal, with some evidence of delayed maturation. However, in adulthood, Sertoli cells (SC) in areas lacking germ cells (Sertoli cell-only [SCO] tubules) often exhibited immature features, especially in cryptorchid testes. Sertoli cells in DBP-exposed animals supported fewer germ cells during puberty, but this normalized in scrotal testes by adulthood. Scrotal and especially cryptorchid testes from DBP-exposed animals exhibited abnormalities (SCO tubules, focal dysgenetic areas) at all postnatal ages. Cryptorchid testes from DBP-exposed animals exhibited more Sertoli cell abnormalities at Day 25 compared with scrotal testes, perhaps indicating more severe underlying Sertoli cell malfunction in these testes. Our findings support the concept of altered Sertoli cell development in TDS, especially in cryptorchid testes, but show that maturational defects in Sertoli cells in adulthood most commonly reflect secondary dedifferentiation in absence of germ cells.
Authors:
Gary R Hutchison; Hayley M Scott; Marion Walker; Chris McKinnell; Diana Ferrara; I Kim Mahood; Richard M Sharpe
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2007-10-10
Journal Detail:
Title:  Biology of reproduction     Volume:  78     ISSN:  0006-3363     ISO Abbreviation:  Biol. Reprod.     Publication Date:  2008 Feb 
Date Detail:
Created Date:  2008-01-29     Completed Date:  2008-03-25     Revised Date:  2014-02-19    
Medline Journal Info:
Nlm Unique ID:  0207224     Medline TA:  Biol Reprod     Country:  United States    
Other Details:
Languages:  eng     Pagination:  352-60     Citation Subset:  IM    
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MeSH Terms
Descriptor/Qualifier:
Animals
Biological Markers / analysis,  metabolism
Cell Count
Cryptorchidism / chemically induced,  pathology*
Dibutyl Phthalate / toxicity
Disease Models, Animal
Follicle Stimulating Hormone / blood
Gonadal Dysgenesis / chemically induced,  pathology*
Inhibins / blood
Male
Organ Size
Plasticizers / toxicity
Proteins / analysis,  metabolism
Rats
Rats, Wistar
Sertoli Cells / drug effects,  pathology*,  physiology
Spermatogonia / cytology,  physiology
Syndrome
Testis / abnormalities*,  pathology*
Testosterone / blood
Grant Support
ID/Acronym/Agency:
MC_U127684422//Medical Research Council
Chemical
Reg. No./Substance:
0/Biological Markers; 0/Plasticizers; 0/Proteins; 2286E5R2KE/Dibutyl Phthalate; 3XMK78S47O/Testosterone; 57285-09-3/Inhibins; 9002-68-0/Follicle Stimulating Hormone

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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