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dc.contributor.advisorNagel, Susan C.eng
dc.contributor.authorPelch, Katherine Eileeneng
dc.date.issued2011eng
dc.date.submitted2011 Falleng
dc.descriptionTitle from PDF of title page (University of Missouri--Columbia, viewed on May 31, 2012).eng
dc.descriptionThe entire thesis text is included in the research.pdf file; the official abstract appears in the short.pdf file; a non-technical public abstract appears in the public.pdf file.eng
dc.descriptionDissertation advisor: Dr. Susan Nageleng
dc.descriptionVita.eng
dc.descriptionIncludes bibliographical references.eng
dc.descriptionDissertations, Academic -- University of Missouri--Columbia -- Biological sciences.eng
dc.descriptionPh. D. University of Missouri-Columbia 2011.eng
dc.description"December 2011"eng
dc.description.abstract[ACCESS RESTRICTED TO THE UNIVERSITY OF MISSOURI AT AUTHOR'S REQUEST.] Xenoestrogens (XE) are chemicals in the environment that mimic the body's natural steroidal estrogens. Developmental exposure to XE may interfere with normal hormonal signaling and result in altered disease susceptibility in adulthood. I used mouse models to examine the effects on three disease endpoints of developmental exposure to three relevant XE: bisphenol A, a ubiquitous chemical found in many food packaging and plastic products; ethinyl estradiol, the primary component of most oral contraceptive pills; and diethylstilbestrol, a former pharmaceutical that has been linked to increased cancer incidence in women exposed in utero. Endometriosis is an estrogen-dependent, benign gynecological disease. First, using a model of surgically-induced endometriosis, I demonstrated that the altered gene expression profile in mice closely mirrors what is observed in women with the disease. I then used this model to explore the effects of developmental XE exposure on endometriosis. Developmental XE exposure was found to alter the expression of immunomodulatory genes. Second, I examined the effects of developmental XE exposure on adult femoral shape and strength. I found that developmental XE exposure increased femoral length and decreased femoral strength, causing bones to fracture more easily. Third, I found that developmental XE exposure increased mammary gland density and tended to increase intraductal hyperplasia. Importantly these effects were seen within the range of current human exposure. Overall my research demonstrates that developmental programming by XE is linked to increased disease susceptibility in adulthood; exposure to low-environmentally relevant levels of XE may increase the risk of endometriosis, bone fractures, and breast cancer.eng
dc.format.extentxii, 182 pageseng
dc.identifier.oclc872563170eng
dc.identifier.urihttps://hdl.handle.net/10355/14471
dc.identifier.urihttps://doi.org/10.32469/10355/14471eng
dc.languageEnglisheng
dc.publisherUniversity of Missouri--Columbiaeng
dc.relation.ispartofcollectionUniversity of Missouri--Columbia. Graduate School. Theses and Dissertations.eng
dc.rightsAccess is limited to the campuses of the University of Missouri.eng
dc.source.originalSubmitted by University of Missouri--Columbia Graduate School.eng
dc.subjectdevelopmental programmingeng
dc.subjectxenoestrogenseng
dc.subjectbisphenol Aeng
dc.subjectendometriosiseng
dc.subjectethinyl estradioleng
dc.titleDevelopmental programming by xenoestrogenseng
dc.typeThesiseng
thesis.degree.disciplineBiological sciences (MU)eng
thesis.degree.grantorUniversity of Missouri--Columbiaeng
thesis.degree.levelDoctoraleng
thesis.degree.namePh. D.eng


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