This Article Full Text Full Text (PDF) Purchase Article View Shopping Cart Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Copyright Permission Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Savabieasfahani, M. Articles by Padmanabhan, V. Search for Related Content PubMed PubMed Citation Articles by Savabieasfahani, M. Articles by Padmanabhan, V. Pubmed/NCBI databases Compound via MeSH Substance via MeSH Hazardous Substances DB 4,4'-BISPHENOL A BISPHENOL A DISODIUM SALT METHOXYCHLOR Medline Plus Health Information High Risk Pregnancy

Developmental Programming: Differential Effects of Prenatal Exposure to Bisphenol-A or Methoxychlor on Reproductive Function

Departments of Pediatrics and the Reproductive Sciences Program (M.S., O.A., V.P.), University of Michigan, Ann Arbor, Michigan 48109; Wadsworth Center (K.K.), New York State Department of Health, and Department of Environmental Health Sciences, State University of New York at Albany, Albany, New York 12201; and Division of Cell Sciences (N.P.E.), University of Glasgow Veterinary School, Glasgow G61 1QH, United Kingdom

Address all correspondence and requests for reprints to: Vasantha Padmanabhan, Department of Pediatrics, 300 North Ingalls Building, Room 1109 SW, Ann Arbor, Michigan 48109-0404. E-mail: vasantha{at}umich.edu.

Increased occurrence of reproductive disorders has raised concerns regarding the impact of endocrine-disrupting chemicals on reproductive health, especially when such exposure occurs during fetal life. Prenatal testosterone (T) treatment leads to growth retardation, postnatal hypergonadotropism, compromised estradiol-positive feedback, polycystic ovaries, and infertility in the adult. Prenatal dihydrotestosterone treatment failed to affect ovarian morphology or estradiol-positive feedback, suggesting that effects of prenatal T may be facilitated via conversion of T to estradiol, thus raising concerns regarding fetal exposure to estrogenic endocrine-disrupting chemicals. This study tested whether fetal exposure to methoxychlor (MXC) or bisphenol A (BPA) would disrupt cyclicity in the ewe. Suffolk ewes were administered MXC (n = 10), BPA (n = 10) (5 mg/kg·d sc in cotton seed oil) or the vehicle (C; n = 16) from d 30 to 90 of gestation. On d 60 of treatment, maternal MXC concentrations in fat tissue and BPA in blood averaged approximately 200 µg/g fat and 37.4 ± 3.3 ng/ml, respectively. Birth weights of BPA offspring were lower (P < 0.05) relative to C. There was no difference in the time of puberty between groups. BPA females were hypergonadotropic during early postnatal life and ended their breeding season later, compared with C. Characterization of cyclic changes after synchronization with prostaglandin F2 in five C, six MXC, and six BPA females found that the onset of the LH surge was delayed in MXC (P < 0.05) and the LH surge magnitude severely dampened (P < 0.05) in BPA sheep. These findings suggest that prenatal BPA and MXC exposure have long-term differential effects on a variety of reproductive endocrine parameters that could impact fertility.

This article has been cited by other articles:

				J. Chen, K. C. Ahn, N. A. Gee, M. I. Ahmed, A. J. Duleba, L. Zhao, S. J. Gee, B. D. Hammock, and B. L. Lasley Triclocarban Enhances Testosterone Action: A New Type of Endocrine Disruptor? Endocrinology, March 1, 2008; 149(3): 1173 - 1179. [Abstract] [Full Text] [PDF]