PMID- 21177253
OWN - NLM
STAT- MEDLINE
DCOM- 20110617
LR  - 20211020
IS  - 1096-0929 (Electronic)
IS  - 1096-6080 (Print)
IS  - 1096-0929 (Linking)
VI  - 120
IP  - 1
DP  - 2011 Mar
TI  - Dipentyl phthalate dosing during sexual differentiation disrupts fetal testis 
      function and postnatal development of the male Sprague-Dawley rat with greater 
      relative potency than other phthalates.
PG  - 184-93
LID - 10.1093/toxsci/kfq386 [doi]
AB  - Phthalate esters (PEs) constitute a large class of plasticizer compounds that are 
      widely used for many consumer product applications. Ten or more members of the PE 
      class of compounds are known to induce male fetal endocrine toxicity and 
      postnatal reproductive malformations by disrupting androgen production during the 
      sexual differentiation period of development. An early study conducted in the rat 
      pubertal model suggested that dipentyl phthalate (DPeP) may be a more potent 
      testicular toxicant than some more extensively studied phthalates. Regulatory 
      agencies require dose-response and potency data to facilitate risk assessment; 
      however, very little data are currently available for DPeP. The goal of this 
      study was to establish a more comprehensive data set for DPeP, focusing on 
      dose-response and potency information for fetal and postnatal male reproductive 
      endpoints. We dosed pregnant rats on gestational day (GD) 17 or GD 14-18 and 
      subsequently evaluated fetal testicular testosterone (T) production on GD 17.5 
      and GD 18, respectively. We also dosed pregnant rats on GD 8-18 and evaluated 
      early postnatal endpoints in male offspring. Comparison of these data to data 
      previously obtained under similar conditions for di (2-ethylhexyl) phthalate 
      indicates that DPeP is approximately eightfold more potent in reducing fetal T 
      production and two- to threefold more potent in inducing development of early 
      postnatal male reproductive malformations. Additionally, fetal testicular T 
      production was more sensitive to inhibitory effects of DPeP exposure than was 
      gene expression of target genes involved in male reproductive development, 
      supporting the use of this endpoint as a critical effect in the risk assessment 
      process.
FAU - Hannas, Bethany R
AU  - Hannas BR
AD  - National Research Council Fellowship Program, National Health and Environmental 
      Effects Laboratory, Office of Research and Development, U.S. Environmental 
      Protection Agency, Research Triangle Park, North Carolina 27711, USA.
FAU - Furr, Johnathan
AU  - Furr J
FAU - Lambright, Christy S
AU  - Lambright CS
FAU - Wilson, Vickie S
AU  - Wilson VS
FAU - Foster, Paul M D
AU  - Foster PM
FAU - Gray, L Earl Jr
AU  - Gray LE Jr
LA  - eng
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, U.S. Gov't, Non-P.H.S.
DEP - 20101220
PL  - United States
TA  - Toxicol Sci
JT  - Toxicological sciences : an official journal of the Society of Toxicology
JID - 9805461
RN  - 0 (Endocrine Disruptors)
RN  - 0 (Phthalic Acids)
RN  - 131-18-0 (di-n-pentyl phthalate)
SB  - IM
MH  - Animals
MH  - Animals, Newborn
MH  - Dose-Response Relationship, Drug
MH  - Endocrine Disruptors/*toxicity
MH  - Female
MH  - Gene Expression Regulation, Developmental/drug effects
MH  - Gestational Age
MH  - Male
MH  - Phthalic Acids/*toxicity
MH  - Pregnancy
MH  - Prenatal Exposure Delayed Effects/*chemically induced/genetics
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Sex Differentiation/*drug effects/genetics
MH  - Testis/*drug effects/embryology/growth & development/metabolism
PMC - PMC3044206
EDAT- 2010/12/24 06:00
MHDA- 2011/06/18 06:00
PMCR- 2012/03/01
CRDT- 2010/12/24 06:00
PHST- 2010/12/24 06:00 [entrez]
PHST- 2010/12/24 06:00 [pubmed]
PHST- 2011/06/18 06:00 [medline]
PHST- 2012/03/01 00:00 [pmc-release]
AID - kfq386 [pii]
AID - 10.1093/toxsci/kfq386 [doi]
PST - ppublish
SO  - Toxicol Sci. 2011 Mar;120(1):184-93. doi: 10.1093/toxsci/kfq386. Epub 2010 Dec 
      20.