Assessment of the Developmental Toxicity, Metabolism, and Placental Transfer of Di-n-butyl Phthalate Administered to Pregnant Rats

Saillenfait, Anne-Marie; Payan, Jean-Paul; Fabry, J.; Beydon, Dominique; Langonné, Isabelle; Gallissot, F.; Sabaté, Jean-Philippe

doi:10.1006/toxs.1998.2518

Cited by 39 publications

(39 citation statements)

References 46 publications

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“…But one should consider that even transient disruption of normal thyroid homeostasis will lead to disastrous outcomes, especially in the developing nervous system (5). And what is worse, DBP and DEHP can readily cross the placenta and are developmental and reproductive toxicants in laboratory animals (34,35). At present, we have no reliable information about whether the level of TR antagonistic activity in drinking water can affect human thyroid hormone system.…”

Section: Resultsmentioning

confidence: 99%

Dibutyl Phthalate Contributes to the Thyroid Receptor Antagonistic Activity in Drinking Water Processes

Wang

Zhou

et al. 2010

Environ. Sci. Technol.

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It has long been recognized that thyroid hormone (TH) is essential for normal brain development in both humans and animals, and there is growing evidence that environmental chemicals can disrupt the thyroid system. In the present work, we used a two-hybrid yeast assay to screen for agonistic or antagonistic thyroid receptor (TR) mediated effects in drinking waters. We found no TR agonistic, but TR antagonistic activities in all samples from the drinking water processes. The TR antagonistic activities in organic extracts of water samples were then calibrated regarding to a known TR-inhibitor, NH3, and were expressed as the NH3 equivalents (TEQbio). The observed TEQbio in waters ranged from 180.8 ( 24.8 to 280.2 ( 48.2 µg/L NH3. To identify the specific compounds responsible for TR disrupting activities, the concentrations of potentially thyroid-disrupting chemicals including organochlorine pesticides (OCPs), phenols, and phthalates in organic extracts were quantitatively determined and their toxic equivalents with respect to NH3 (TEQcal) were estimated from their concentrationdependent relationships, respectively, using the same set of bioassays. Based on the TEQ approach, it was revealed that dibutyl phthalate (DBP) accounted for 53.7 ( 8.2% to 105.5 ( 16.7% of TEQbio. There was no effective removal of these potential thyroid disrupting substances throughout drinking water treatment processes.

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Section: Resultsmentioning

confidence: 99%

Dibutyl Phthalate Contributes to the Thyroid Receptor Antagonistic Activity in Drinking Water Processes

Wang

Zhou

et al. 2010

Environ. Sci. Technol.

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“…We observed that after administration of a single oral dose of 0.5 or 1.5 g [ 14 C] di-n-butyl phthalate/kg (1.8 and 5.6 mmol/kg, respectively) to Sprague-Dawley rats on Day 14, mono-n-butyl phthalate and its glucuronide accounted for about 50-95% of the radioactivity recovered in maternal plasma and embryonic tissues, whereas unchanged di-n-butyl phthalate generally accounted for less than 1% (Saillenfait et al 1998).…”

Section: Discussionmentioning

confidence: 99%

“…The selection of the doses was based on the results of our previous study in which administration of di-n-butyl phthalate to Sprague-Dawley rats by gavage on Day 14 increased the incidence of postimplantation loss at 1.5 g/kg (5.4 mmol/kg) and above. There were no indications of any adverse effects on embryonic and foetal development at 0.5 g/ kg (Saillenfait et al 1998). We also took into account the studies of Ema et al (1994Ema et al ( & 1996 who found an increased number of resorptions following gastric intubation of Wistar rats with 0.75 g di-nbutyl phthalate/kg or 0.625 g mono-n-butyl phthalate/kg (2.8 mmol/ kg) from day 10 through 12 of gestation.…”

Section: Methodsmentioning

confidence: 99%

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Effects of Mono‐n‐butyl Phthalate on the Development of Rat Embryos: In vivo and in vitro Observations

Saillenfait¹,

Langonné²,

Leheup

2001

Pharmacology & Toxicology

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The present study was conducted to further characterize the embryotoxic effects mono-n-butyl phthalate, a major metabolite of the plasticizer di-n-butyl phthalate, and evaluate its role in the developmental toxicity of di-n-butyl phthalate. The embryotoxic effects of mono-n-butyl phthalate were compared to those of the parent compound di-n-butyl phthalate after a single oral administration of 1.8, 3.6, 5.4, or 7.2 mmol/kg di-n-butyl phthalate or mono-n-butyl phthalate to Sprague-Dawley rats on gestational day 10 (Day 10). Embryos were evaluated for growth and development on Day 12. Both chemicals induced concentration-dependent developmental toxicity (i.e. decreased growth and malformations) which became apparent at 3.6 mmol/kg. Di-n-butyl phthalate and mono-n-butyl phthalate were approximately equally potent and produced qualitatively similar dysmorphogenic effects. Macroscopically, the most common malformations involved the prosencephalon, the optic system, and the mandibular and maxillary processes. In addition, the embryotoxic potential of mono-n-butyl phthalate was evaluated in vitro using the rat whole embryo culture system. Day 10 embryos were cultured for 48 hr in the presence of 0.5 to 5 mM mono-n-butyl phthalate and were then evaluated as the embryos grown in utero. Mono-n-butyl phthalate was a potent direct acting embryotoxicant, causing concentration-related growth retardation and dysmorphogenesis. The spectrum of morphological defects observed in mono-n-butyl phthalate-exposed embryos in vitro was comparable to those seen in vivo in the embryos at the same developmental stage after maternal administration of di-n-butyl phthalate or mono-n-butyl phthalate. These data provide additional evidence in support of the hypothesis that mono-n-butyl phthalate may be the active species for the developmental toxicity of ingested di-n-butyl phthalate in rats.

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“…Yes, phthalates do cross the placenta during pregnancy and expose babies. During pregnancy, significant amount of phthalates and their metabolites are transferred to the fetus (Calafat et al, 2004;Fennell et al, 2004;Saillenfait et al, 1998). Human placenta is not an effective barrier for fetal exposure to phthalates.…”

Section: Q My Child Frequent Chews On Toys Can This Lead To Phthalamentioning

confidence: 99%

Phthalates in food and medical devices

Chou

Wright

2006

J. Med. Toxicol.

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Assessment of the Developmental Toxicity, Metabolism, and Placental Transfer of Di-n-butyl Phthalate Administered to Pregnant Rats

Cited by 39 publications

References 46 publications

Dibutyl Phthalate Contributes to the Thyroid Receptor Antagonistic Activity in Drinking Water Processes

Dibutyl Phthalate Contributes to the Thyroid Receptor Antagonistic Activity in Drinking Water Processes

Effects of Mono‐n‐butyl Phthalate on the Development of Rat Embryos: In vivo and in vitro Observations

Phthalates in food and medical devices

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