Citation:

Furr, J. AND E. Gray. Postnatal effects of dipentyl phthalate on male reproductive development. Presented at Society of Toxicology Meeting, March 10 - 14, 2013.

Impact/Purpose:

This abstract will be presented at the Society of Toxicology meeting March 10-14, 2013, San Antonio, TX

Description:

We conducted several in utero, ex vivo and in vitro studies to characterize the relative potencies of a series of phthalates on fetal rat testis testosterone production and gene expression. Dipentyl phthalate (DPeP) was the most potent of the active chemicals in its effect on fetal testis endocrine function. Although these studies have pointed to the overall potency of DPeP, little literature exists defining its dose-response curve in vivo. The objective of this study was to determine if the potency of DPeP on fetal testis endocrine function was predictive of the ability of the chemical to induce reproductive tract malformations in male rats. We treated timed-pregnant Sprague-Dawley rats 0, 11, 33, 100 or 300 mg DPeP/kg/d, from GD 8-18 and examined the postnatal development of the male offspring. Male offspring of treated dams displayed decreased AGD, increased nipple retention, incomplete preputial separation, decreased sperm production, hypospadias, undescended testes, malformations of the testes, ventral prostate, and seminal vesicles, reduced body weight (300 mg/kg/day) and reduced postnatal survival. Phthalate syndrome (PS) malformations were seen in about 9%, 44% and 100% of the F1 male offspring at 33, 100 and 300 mg/kg/d, dosage levels that reduced fetal T production by 35%, 77% and 93% respectively. Also of note were skull malformations in highest treatment group in the form of malocclusions and incomplete zygomatic ossification. These results indicate the DPeP is about 3.5 fold more potent in inducing the PS in F1 male rats than is DEHP and demonstrate that the relative potencies for disrupting fetal testis endocrine function can be used to predict some the postnatal reproductive effects of this class of endocrine disruptors. Disclaimer: This abstract does not reflect USEPA policy. Supported in part by NTP/NIEHS IA# RW-75-92285501.

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