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Biology of Reproduction, Vol 21, 491-495, Copyright © 1979 by Society for the Study of Reproduction
1 Department of Obstetrics and Gynecology,
and Department of Anatomy,
School of Medicine
West Virginia University,
Morgantown, West Virginia 26506 Absorption of estrogen by an antiserum against estradiol (ASE) and replacement with diethylstilbestrol (DES) were used to study the role of the early preovulatory rise of estrogen during
delayed ovulation on the subsequent increase in abnormal morphological development of the
embryos. The study contained 4 treatment groups: 1) control; 2) pentobarbital sodium (Nembutal)-induced delay of ovulation for 48 h; 3) delay of ovulation plus ASE treatment on the first 2 days
of the estrous cycle; and 4) DES treatment during the first 2 days of the cycle in addition to
treatment with ASE and delay of ovulation. The ASE used did not bind DES. Following mating,
rats were killed at Day 4 (blastocyst stage) or Day 11 (midgestation) to assess development of
embryos. A 48 h delay of ovulation, as reported previously, produced abnormal development and retarded
growth of the embryos at both stages of development (P<0.05). Implantation rate was decreased,
while embryonic death was increased (P<0.05). All of these detrimental effects were reversed by
ASE, while DES reinitiated these events in ASE treated rats. The results suggest that the early rise
or prolonged elevation of preovulatory levels of estrogen in relation to the time of ovulation is
responsible for alterations in the oocyte and intrauterine environment which result in subsequent
abnormal development and embryonic death following delayed ovulation.
Note:
ACKNOWLEDGMENTS
We thank Mrs. Diana Kirkpatrick-Keller for her
excellent technical assistance which made this study
possible and Dr. W. V. Thayne for statistical analysis.
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