Developmentally arrested oviduct: A structural and functional defect in mice following prenatal exposure to diethylstilbestrol

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Abstract
To determine the effects of exposure to diethylstilbestrol (DES) on the developing oviduct, timed pregnant CD‐1 mice were treated with DES (10–100 μg/kg subcutaneous) on days 9–16 of gestation. Prenatal DES‐exposed and age‐matched control mice were sacrificed from day 16 of gestation to 15 weeks of age and oviductal development was compared. Following prenatal exposure to DES (100 μg/kg), the oviduct at all ages examined was uncoiled and shorter, closely adherent to and wrapped around the ovary in an anatomical configuration similar to the fetal mouse. In addition, the demarcation between the oviduct and uterus was not readily apparent. Histological changes in the DES (100 μg/kg) oviduct as compared with control at 10–15 weeks of age included a proliferation of columnar epithelium lining the lumen with gland formation extending into the underlying stroma, absence of or a reduced amount of fimbrial tissue, increased thickness of the muscular wall, and inflammatory cell infiltration. Also, as a functional test of uterotubal junction integrity, Coomassie Blue dye was injected into the uterus. The control uterotubal junction confined the fluid to the uterus. In 80% and 100% of the animals exposed prenatally to DES (10 and 100 μg/kg, respectively), independent of the extent of the gross abnormality, the dye readily flowed into the oviduct and filled the ovarian bursa. We conclude that prenatal DES exposure can alter fetal development of the mouse oviduct, resulting in an apparent developmental arrest and functional disruption of the integrity of the uterotubal junction. The fetal like configuration of the ovary, oviduct, and uterus suggests the term developmentally arrested oviduct (DAO).