Developmental exposure to bisphenol A alters the differentiation and functional response of the adult rat uterus to estrogen treatment |
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Affiliation: | 1. Chemistry and Life Sciences College, Key Laboratory of Wildlife Biotechnology and Conservation and Utilization of Zhejiang Province, Zhejiang Normal University, PR China;2. Zhejiang Provincial Key Laboratory of Ecology, Zhejiang Normal University, PR China;1. School of Biomedicine Sciences, Chengdu Medical College, Chengdu, China;2. School of Basic Medical Sciences, Chengdu Medical College, Chengdu, China;3. Center of Science and Research, Chengdu Medical College, Chengdu, China;4. Department of Microbial and Biochemical Pharmacy, School of Pharmaceutical Sciences, Sun Yat-sen University, Guangzhou, China;1. Bond Life Sciences Center, University of Missouri, Columbia, MO 65211, United States;2. Biomedical Sciences, University of Missouri, Columbia, MO 65211, United States;3. Agriculture Experimental Station-Statistics, University of Missouri, Columbia, MO 65211, United States;4. Department of Animal Science, Texas A&M University, College Station, TX 77843, United States;5. Division of Biochemical Toxicology, National Center for Toxicological Research/Food and Drug Administration, Jefferson, AR 72079, United States;6. Office of Scientific Coordination, National Center for Toxicological Research/Food and Drug Administration, Jefferson, AR 72079, United States;7. Division of Neurotoxicology, National Center for Toxicological Research/Food and Drug Administration, Jefferson, AR 72079, United States;8. Genetics Area Program, University of Missouri, Columbia, MO 65211, United States;9. Thompson Center for Autism and Neurobehavioral Disorders, University of Missouri, Columbia, MO 65211, United States;1. Neuroscience Program, University of Illinois at Urbana–Champaign, Champaign, IL 61820, United States;2. Department of Psychology, University of Illinois at Urbana–Champaign, Champaign, IL 61820, United States;3. Comparative Biosciences, University of Illinois at Urbana–Champaign, Champaign, IL 61820, United States;1. Division of Biochemical Toxicology, National Center for Toxicological Research, Food and Drug Administration, 3900 NCTR Road, Jefferson, AR 72079, USA;2. Division of Bioinformatics and Biostatistics, National Center for Toxicological Research, Food and Drug Administration, 3900 NCTR Road, Jefferson, AR 72079, USA;3. Division of Systems Biology, National Center for Toxicological Research, Food and Drug Administration, 3900 NCTR Road, Jefferson, AR 72079, USA;4. Office of Scientific Coordination, National Center for Toxicological Research, Food and Drug Administration, 3900 NCTR Road, Jefferson, AR 72079, USA |
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Abstract: | We assessed the long-term effect of perinatal exposure to bisphenol A (BPA) on the rat uterus and the uterine response to estrogen (E2) replacement therapy. BPA (0.5 or 50 μg/kg/day) was administered in the drinking water from gestational day 9 until weaning. We studied the uterus of female offspring on postnatal day (PND) 90 and 360, and the uterine E2 response on PND460 (PND460-E2). On PND90, BPA-exposed rats showed altered glandular proliferation and α-actin expression. On PND360, BPA exposure increased the incidence of abnormalities in the luminal and glandular epithelium. On PND460-E2, the multiplicity of glands with squamous metaplasia increased in BPA50 while the incidence of glands with daughter glands increased in BPA0.5. The expression of steroid receptors, p63 and IGF-I was modified in BPA-exposed rats on PND460-E2. The long-lasting effects of perinatal exposure to BPA included induction of abnormalities in uterine tissue and altered response to E2 replacement therapy. |
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Keywords: | Bisphenol A Rat Uterus Uterine glands Steroid receptors p63 |
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