A number of well-known cases of endocrine disruption (ED) in wildlife populations have been documented. In most instances, a single class of compounds (commonly xenoestrogens or aromatic hydrocarbons) has been identified as the probable cause of the ED. However, knowledge of potential ED caused by exposure to low level, environmentally relevant mixtures is poor. The current proposal is developed from previous observations made by this laboratory on a sentinel species, the freshwater turtle, Chrysemys picta. Studies conducted in the area of the Massachusetts Military Reservation (MMR), a Superfund site, have revealed significant reproductive deficits in turtles from a test site potentially impacted by a contaminated groundwater plumes. Animals are slow to mature, have a reduced oocyte cohort, reduced sperm number, lower plasma estradiol and reduced vitellogenin levels compared to animals from a control site. The hypothesis is 1) that the reproductive deficits are the result of past and/or continuous exposure to unidentified endocrine disruptors, 2) that the endocrine disruptors interfere with (a) the hypothalamic-pituitary-gonadal-target organ axis at one or more sites or (b) directly or indirectly with the process of gametogenesis.
The Specific Aims are as follows: 1a. Determine whether the hepatic vitallogenin response to estradiol is impaired, 1b. Determine the gonadal response to gonadotropin in vivo, 1c. Determine pituitary responsiveness to varying amounts of gonadotropin releasing hormone (GnRH), 2. Determine in adult, juvenile and embryonic turtles, from the reference and impacted sites, whether the reduced number of small oocytes and sperm are due to impaired germ cell migration, impaired oogonial or spermatogonial proliferation, reduced gonadotropin levels or to an enhanced rate of apoptosis. In vivo and in vitro studies of liver, gonadal and hypothalamic response to hormone stimuli will be assessed using a variety of endpoints (vitellogenin, steroid synthesis and gonadotropin secretion).
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