US EPA

1333128 

Journal Article 

Abstract 

Antiandrogenic effects of dibutyl phthalate and its metabolite, monobutyl phthalate 

Ema, M 

2002 

Yes 

Congenital Anomalies
ISSN: 0914-3505
EISSN: 1741-4520 

42 

3 

234 

English 

is related to other part(s) 675075 , in rats
is part of a larger document 4997274 42nd Annual Meeting of the Japanese Teratology Society abstracts

The developmental toxicity of dibutyl phthalate (DBP) and its metabolite, monobutyl phthalate (MBuP), was determined in Wistar rats. Oral DBP on days 7-15 of pregnancy caused a decrease in the maternal body weight gain, increased postimplantation loss, and decrease in fetal weight at 630 mg/kg and higher and caused an increase in the incidence of fetuses with malformations at 750 mg/kg. Oral MBuP on days 7-15 of pregnancy caused a decreased maternal body weight gain, increased number of postimplantation loss, low weight of fetuses, and increased incidence of fetuses with malformations at 500 mg/kg and higher. Oral DBP on days 15-17 of pregnancy caused a decrease in the anogenital distance (AGD) in male fetuses and increased incidence of fetuses with undescended testes at 500 mg/kg and higher, caused a decrease in the maternal body weight gain at 1000 mg/kg and higher, and caused increased postimplantation loss and low fetal weight at 1500 mg/kg. Oral MBuP on days 15-17 of pregnancy caused a decreased AGD in male fetuses and increased incidence of fetuses with undescended testes at 250 mg/kg and higher, caused a decreased maternal body weight gain and increased number of postimplantation loss at 500 mg/kg and higher, and caused a low fetal weight at 750 mg/kg. No effects of DBP and MBuP on the AGD were found in female fetuses. The spectrum of fetal malformations, dependence on gestational days of treatment on the manifestation of teratogenicity, and decreased AGD and increased incidence of fetuses with undescended testes in male fetuses observed after the administration of DBP were in good agreement with those observed after the administration of MBuP. These findings suggest that MBuP may be responsible for the induction of the developmental toxic effects of DBP. The doses that produced a decrease in the AGD and undescended testes in male offspring were lower than those producing maternal toxicity, fetal malformations, and postimplantation loss. The male reproductive system may be more susceptible than other organ systems to DBP toxicity after maternal exposure. 

Pregnancy; Animal; Rats; Male; Female; Rats, Wistar; Dibutyl Phthalate/TOXICITY; Androgen Antagonists/TOXICITY; Phthalic Acids/TOXICITY; Prenatal Exposure Delayed Effects; Abnormalities, Drug-Induced/EMBRYOLOGY; Cryptorchidism/EMBRYOLOGY; Cryptorchidism/CHEMICALLY INDUCED; Postimplantation Phase/DRUG EFFECTS; Administration, Oral; Sex Factors; Dose-Response Relationship, Drug; 84-74-2; NO CAS RN; 131-70-4 

The Japanese Teratology Society 42nd Annual Meeting 

July 10-12, 2002