title: In utero and lactational exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin alters postnatal development of seminal vesicle epithelium.
abstract: 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) has been shown to alter male reproductive development of laboratory animals through in utero and lactational exposure. As a result of exposure, the accessory glands of the male reproductive tract, including the seminal vesicle, are decreased in size as determined by total weight of the tissue. Analysis of seminal vesicle weights over time suggests that the changes may be transient. Administration of 1.0 microg/kg TCDD during gestation caused a significant decrease in seminal vesicle weights of offspring 8-11 months of age. We examined the effects of TCDD on seminal vesicles from rats exposed in utero and lactationally. Pregnant Long Evans rats were gavaged on gestation day 15 with 1.0 microg/kg TCDD in corn oil. Male pups were euthanized and necropsied on postnatal days (PND) 15, 25, 32, 49, 63, and 120. Seminal vesicles were weighed and then fixed in 10% neutral buffered formalin and processed for microscopic examination. Seminal vesicle weights were not significantly decreased until PND 32. Androgen receptor mRNA expression in PND 25 seminal vesicles was not different from control. In the present study, TCDD exposure decreased seminal vesicle epithelial branching and differentiation. Control epithelial cells had tall columnar morphology with relatively abundant cytoplasm, whereas TCDD-treated cells had rounded nuclei and less cytoplasm. In addition, immunolocalization of proliferating nuclear antigen was confined to undifferentiated basal epithelial cells of controls but was found in both basal and luminal cells of the treated seminal vesicle. Results indicate that the TCDD-induced impaired growth of the rat seminal vesicles is associated with a dramatic decrease in the development of the epithelium.
authors.affiliation: Curriculum in Toxicology, University of North Carolina, Chapel Hill 27599, USA. hamm.jonathan@epamail.epa.gov
authors.forename: J T
authors.initials: JT
authors.lastname: Hamm
authors.forename: B R
authors.initials: BR
authors.lastname: Sparrow
authors.forename: D
authors.initials: D
authors.lastname: Wolf
authors.forename: L S
authors.initials: LS
authors.lastname: Birnbaum
mesh_terms: D000284:Administration, Oral; D000818:Animals; D000831:Animals, Newborn; D001835:Body Weight / Q000187:drug effects; D017931:DNA Primers / Q000737:chemistry; D004785:Environmental Pollutants / Q000633:toxicity*; D004848:Epithelium / Q000187:drug effects / Q000254:growth & development / Q000473:pathology; D005260:Female; D007774:Lactation; D008297:Male; D009929:Organ Size / Q000187:drug effects; D000072317:Polychlorinated Dibenzodioxins / Q000633:toxicity*; D016133:Polymerase Chain Reaction; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects; D012333:RNA, Messenger / Q000378:metabolism; D051381:Rats; D020318:Rats, Long-Evans; D011944:Receptors, Androgen / Q000235:genetics / Q000378:metabolism; D012669:Seminal Vesicles / Q000187:drug effects* / Q000254:growth & development / Q000378:metabolism / Q000473:pathology
chemical_list: D017931:DNA Primers; D004785:Environmental Pollutants; D000072317:Polychlorinated Dibenzodioxins; D012333:RNA, Messenger; D011944:Receptors, Androgen