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2007 FIR Mini Symposium Details
Our Chemically Modified Environment: What is happening to reproductive homeostasis?
June 1, 2007, 2-5 PM
Speck Auditorium, Rowe Laboratory
Full Symposium Schedule
Pat Hunt of Washington State University was led to the effects of estrogen mimics on reproductive health through an enlightening accident. In 1988, Hunt and her colleagues, then at Case Western Reserve University, were subjecting mouse eggs to an estrogenic substance to test whether the eggs go through a rapid growth phase prior to ovulation. Suddenly, they observed a dramatic increase in the number of eggs that had divided incorrectly, resulting in aneuploidy in the daughter cells. They traced the problem to damaged polycarbonate mouse cages and water bottles, which were leaching bisphenol A1.
At the FIR symposium in June, Hunt presented newer research from her lab that demonstrates a “grandmaternal” effect: Low-dose exposure to BPA during pregnancy disturbs the eggs that are developing in the female fetus2. “So three generations are affected: the pregnant mother, her daughter, and the eggs that will be her grandchildren,” Hunt says.
It’s one of the very new and disconcerting things we are finding,” David Albertini says. “Both during gestation and even probably prior to gestation, exposures like this may not interrupt the process of reproduction, but will deleteriously affect the offspring.”
Karla Hutt from Albertini’s laboratory at University of Kansas Medical Center discussed their work on a compound called TCDD, which is present in the environment and in human beings. “We dose animals (rats) at ‘environmentally relevant’ doses, rather than toxic doses,” he says. “The doses are so relevant that they do not interfere with reproduction in these animals, but they give birth to rats who are prone to illnesses later in life. These small doses do affect the way the nucleus of the embryo cells is organized.3”
Carlos Sonnenschein of Tufts Medical School gave an overview of his research on environmental estrogens since his co-discovery (again, accidentally) of an estrogenic compound, nonylphenol. Sonnenschein, Ana Soto and their colleagues had been studying how the sex steroids, estrogen and androgen, regulate the proliferation of their target cells. When they unexpectedly observed cell proliferation in the absence of a sex steroid, they discovered that nonylphenol, which was being released from the plastic tubes used to store culture media components, was an estrogen mimic4. Sonnenschein also discussed the E-SCREEN assay, a test for estrogenicity that his laboratory developed5, and his work to uncover the relationship between environmental estrogen mimics and breast and prostate cancers.6
References
- Hunt, P.A., et. al. (2003). Bisphenol A exposure causes meiotic aneuploidy in the female mouse. Current Biology (13)7: 546-553.
- Susairjo, M., Hassold, T.J., Freeman, E.J. and Hunt, P.A. (2007). Bisphenol A exposure in utero disrupts early oogenesis in the mouse. PLoS Genet 3(1): e5 doi:10.1371/journal.pgen.0030005.
- Hutt, K., Albertini, D.F., and Petroff, P. (2007). Effects of TCDD on pre-implantation embryo development in the rat: the epigenetic dilemma. Annual Meeting for the Society for the Study of Reproduction, San Antonio.
- Soto, A. M., Wray, J., Justicia, H. and Sonnenschein, C. (1991). p-Nonyl phenol: an estrogenic xenobiotic released from modified polystyrene. Environ. Health Perspect. 92:167-173.
- Soto, A. M., Sonnenschein, C., Chung, K. L., Fernandez, M. F., Olea, N. and Olea Serrano, F. (1995). The E-SCREEN assay as a tool to identify estrogens: an update on estrogenic environmental pollutants. Environ. Health Perspect. 103, Supplement 7, 113-122.
- Murray, T.J., Maffini, M.V., Ucci, A.A., Sonnenschein, C, Soto, A.M. (2007). Induction of mammary gland ductal hyperplasias and carcinoma in situ following fetal bisphenol A exposure. Reprod. Toxicol. Apr-May; 23(3):383-390.
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