Linked Life Data

17289843

Source:http://linkedlifedata.com/resource/pubmed/id/17289843

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
2007-4-20
pubmed:abstractText
This study sought to establish whether reduced androgen levels/action in the fetal rat testis induced by di(n-butyl) phthalate (DBP) contributes to dysgenetic features, namely reduced Sertoli cell number, occurrence of multinucleated gonocytes (MNG), and Leydig cell aggregation. Pregnant rats were administered treatments or cotreatments designed to manipulate testosterone levels [DBP, testosterone propionate (TP)] or action [flutamide, 7,12-dimethyl-benz[a]anthracene (DMBA)]. The aforementioned end points were analyzed and related to intratesticular testosterone (ITT) levels and peripheral androgen action (anogenital distance). Dysgenetic features were also evaluated in mice with inactivation of the androgen receptor (testicular feminized or ARKO mice). Exposure to DBP alone, or combined with flutamide, DMBA, or TP, resulted in reduced Sertoli cell number and ITT levels, as did exposure to TP alone; coadministration of DBP + TP caused the most severe reduction in both parameters. A positive correlation between ITT levels and Sertoli cell number was found (r = 0.791; P = 0.019). Similarly, exposure to DBP alone, or as a cotreatment, significantly increased occurrence of MNG and Leydig cell aggregation, and these were negatively correlated with ITT levels. Exposure to flutamide or DMBA alone had no significant effect on these dysgenetic end points. These findings suggest that reduced ITT decreases fetal Sertoli cell numbers and might be involved in Leydig cell aggregation and MNG. However, of these three end points, only Sertoli cell number was affected significantly in ARKO/testicular feminized mice with absent androgen action. Therefore, induction of MNG and Leydig cell aggregation might result from DBP-induced effects other than suppression of ITT levels.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
0013-7227
pubmed:author
pubmed:issnType
Print
pubmed:volume
148
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
2027-36
pubmed:meshHeading
pubmed-meshheading:17289843-9,10-Dimethyl-1,2-benzanthracene, pubmed-meshheading:17289843-Androgen Antagonists, pubmed-meshheading:17289843-Animals, pubmed-meshheading:17289843-Body Weight, pubmed-meshheading:17289843-Carcinogens, pubmed-meshheading:17289843-Dibutyl Phthalate, pubmed-meshheading:17289843-Female, pubmed-meshheading:17289843-Feminization, pubmed-meshheading:17289843-Flutamide, pubmed-meshheading:17289843-Giant Cells, pubmed-meshheading:17289843-Gonadal Dysgenesis, pubmed-meshheading:17289843-Leydig Cells, pubmed-meshheading:17289843-Male, pubmed-meshheading:17289843-Mice, pubmed-meshheading:17289843-Mice, Knockout, pubmed-meshheading:17289843-Organ Size, pubmed-meshheading:17289843-Pregnancy, pubmed-meshheading:17289843-Prenatal Exposure Delayed Effects, pubmed-meshheading:17289843-Rats, pubmed-meshheading:17289843-Rats, Wistar, pubmed-meshheading:17289843-Receptors, Androgen, pubmed-meshheading:17289843-Sertoli Cells, pubmed-meshheading:17289843-Testis, pubmed-meshheading:17289843-Testosterone
pubmed:year
2007
pubmed:articleTitle
Role of androgens in fetal testis development and dysgenesis.
pubmed:affiliation
Medical Research Council Human Reproductive Sciences Unit, Centre for Reproductive Biology, The Queen's Medical Research Institute, 47 Little France Crescent, Edinburgh EH16 4TJ, UK.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't