Abstract
Chronic exposure to environmentally relevant concentrations of the aryl hydrocarbon receptor-specific toxicant 2,3,7,8-tetrachlorodibenzo-pdioxin (TCDD) causes premature reproductive senescence in female rats through what appear to be preferential actions on the ovary. In an effort to definitively localize these chronic actions of TCDD on the female reproductive axis, adult pregnant Lewis rat dams (n=24) were dosed with corn oil vehicle or TCDD (50 ng kg-1 wk-1) to provide in utero and lactational (IUL) exposure to pups. Female pups were weaned on postnatal day 21 and dosed with TCDD or vehicle weekly. Ovaries from donor animals treated with TCDD or vehicle were harvested at 3 weeks of age and transplanted into the ovarian bursae of similarly treated recipient females. Following ovary transplantation, rats (n=6–8 per group) received weekly TCDD or vehicle until reproductive senescence in a factorial design for IUL vs. adult and ovarian vs. extraovarian exposure to TCDD. Beginning at vaginal opening, reproductive cyclicity was monitored by vaginal cytology for 10 days each month. Blood samples were collected across the estrous cycle at 3 and 8–9 months of age. Procedural controls included naïve and sham-operated females treated with TCDD or vehicle. Ovary transplantation resulted in precocious vaginal opening regardless of treatment group. Ovarian cyclicity following transplantation was less regular than for sham or naïve controls. IUL ovarian exposure to TCDD was more detrimental to subsequent reproductive cyclicity than extraovarian and adult exposures. The immature ovary appears to be a sensitive developmental target of the AhR during environmental endocrine disruption. (platform)
Published Version
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call