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Biology of Reproduction, Vol 24, 249-256, Copyright © 1981 by Society for the Study of Reproduction
1 Department of Physiology and Biophysics,
University of Illinois at the Medical Center,
Chicago, Illinois 60680 To determine the sites of androgen and estradiol production in the second half of pregnancy,
pregnant rats were hypophysectomized or hypophysectomized and hysterectomized on Day 12.
After hypophysectomy, the luteal weight, the concentration of androgen and estradiol in corpora
lutea, and serum androgen remained at control values on Days 14, 18, and 22. In contrast, by Day
14 the nonluteal tissue atrophied, its estradiol concentration decreased, and serum estradiol declined from 25 ± 1.0 in sham-treated animals to 21 ± 0.3 pg/ml. When the conceptuses were
removed together with the pituitary by hypophysectomy and hysterectomy on Day 12, androgen
and estradiol levels in the serum dropped to barely detectable levels. To determine whether the
placentas secreted androgen or stimulated androgen secretion by other endocrine glands, adrenals,
ovaries, and/or fetuses were removed from rats hypophysectomized on Day 12, and pregnancy was
maintained with progesterone treatment. No decrease in androgen levels in the serum was observed.
Serum androgen remained elevated in all groups in which the placentas remained in utero. When
the placentas were removed, as in hypophysectomized-hysterectomized rats, serum androgen
dropped dramatically. However, while androgen levels remained elevated, serum estradiol declined
after either ovariectomy or fetectomy and a synergism was observed when ovariectomy and fetectomy were combined. These results indicate that the placentas are a source of androgen in the
second half of pregnancy and that the ovaries and fetuses are a site of estradiol production.
Note:
ACKNOWLEDGMENTS
We wish to thank Janet L. Chien for helping with
the radioimmunoassay, Linda Alaniz and Rosemary
Clepper for taking care of the animals, and Mrs.
Bridget Archer for excellent help in typing the manuscript.
We also thank Dr. G. D. Niswender, Colorado
State University, for the androgen and estradiol
antisera.
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