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Biology of Reproduction, Vol 25, 272-280, Copyright © 1981 by Society for the Study of Reproduction
1 MRC Group in Reproductive Biology and Department of Physiology,
The University of Western Ontario,
London, Ontario, Canada N6A 5A5 Use of exogenous gonadotropin to induce ovulation may be associated with reduced fertility
resulting from excessive follicular stimulation. To investigate this problem further a superovulatory
dose of 40 IU PMSG was administered to 29-day-old rats at 0800-0900 h on Day -2 (see text
footnote 4) of the experiment (SOV animals). Control rats received 4 IU PMSG, a dose which induces a physiological number of ovulations followed by a normal pregnancy. A volume of antiserum (a/s) known to inhibit completely the ovarian and uterine weight increasing capacity of 40
IU PMSG was injected i.p. at 1800 h on Day 0 to 50% of the SOV group (SOV a/s animals). Females were then caged with mature fertile males overnight, examined for evidence of mating on
Day 1, and sacrificed at 1030-1230 h on Days 1-5. Tissue and blood were collected for steroid
analyses, and oviducts and uteri were flushed to determine the number and location of embryos.
Animals receiving a/s had higher embryo recovery on Days 4 and 5 compared with SOV animals.
On Day 5 a mean of 10.5 embryos was recovered from SOV a/s animals compared with 8.2 in control rats and 2.4 in SOV animals. On Day 5 most SOV animals had no embryos whereas following
a/s all animals were pregnant and the majority of embryos were in the uterus. In control rats all
embryos were in the uterus on Day 5. Serum and ovarian progesterone levels were 3-4-fold higher
in SOV animals compared with controls, but were unchanged by administration of a/s, whereas
estradiol-17
in both serum and ovaries was drastically reduced to levels close to those observed in
control rats within 18 h of administration of a/s. These results suggest that early embryo loss
after superovulation may result, at least in part, from excessive estrogen secretion, probably
arising from remaining follicles. This loss could occur through excessive stimulation of either the
oviductal or uterine environments or both.
Note:
ACKNOWLEDGMENTS
The authors wish to thank Dr. B. G. Miller, Dept.
of Animal Husbandry, University of Sydney, Australia, for valuable discussions during the planning of
these experiments; Dr. N. Birkett, Dept. of Epidemiology and Biostatistics, University of Western
Ontario, Canada, for advice with statistical analyses;
Mr. G. Barbe for advice concerning assays; and Ms. M.
Dobias and Dr. S. Huntley for excellent technical
assistance.
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  L. J. Edwards, K. L. Kind, D. T. Armstrong, and J. G. Thompson Effects of recombinant human follicle-stimulating hormone on embryo development in mice Am J Physiol Endocrinol Metab, May 1, 2005; 288(5): E845 - E851. [Abstract] [Full Text] [PDF]
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 D. Zudova, A. J. Wyrobek, J. Bishop, and F. Marchetti Impaired fertility in T-stock female mice after superovulation Reproduction, November 1, 2004; 128(5): 573 - 581. [Abstract] [Full Text] [PDF]
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 I. Van der Auwera and T. D'Hooghe Superovulation of female mice delays embryonic and fetal development Hum. Reprod., June 1, 2001; 16(6): 1237 - 1243. [Abstract] [Full Text] [PDF]
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