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Biology of Reproduction, Vol 25, 235-243, Copyright © 1981 by Society for the Study of Reproduction
1 Division of Reproductive Biology,
Department of Population Dynamics,
The Johns Hopkins University School of Hygiene and Public Health,
Baltimore, Maryland 21205 Testosterone and estradiol, administered by polydimethylsiloxane (PDS) Silastic implants, act
synergistically to inhibit spermatogenesis. In previous experiments, we examined the effect of
testosterone plus estradiol implants on pituitary and testicular function at a single time interval
after implantation (usually 3 months). In the present study, we killed rats at 4 h intervals (0400,
0800, 1200, 1600, 2000, and 2400 h) on Days 0, 2, 9, 16, 29, and 57 after implanting testosterone-estradiol PDS capsules. We measured serum concentrations of luteinizing hormone, testosterone, and estradiol; testosterone production by in vitro perfused testes; daily sperm production;
and body, testis, epididymal, seminal vesicle, and ventral prostate weights. Luteinizing hormone
was not detectable in the serum 2 days after implanting PDS capsules and remained suppressed
until the end of the study. Testosterone secretion declined to low levels 9 days postimplantation
and remained suppressed until the end of the study. Sperm production was inhibited completely
by 57 days postimplantation. Serum testosterone and estradiol concentrations increased immediately after implantation of the PDS capsules but returned towards control values as Leydig cell
testosterone production declined. Control rats showed a diurnal rhythm in serum testosterone
concentration which had a frequency of 2 cycles per day and an amplitude of 2.2 ng/ml. The
testosterone plus estradiol PDS subdermal implants altered the diurnal rhythm in serum testosterone concentration prior to 29 days of treatment. After 29 days of treatment, the diurnal rhythm in serum testosterone concentration disappeared. These complex changes in the diurnal
rhythm of serum testosterone concentration during the first 29 days were interpreted to mean that
both testicular testosterone production and testosterone metabolism were responsible for maintaining the rhythm in control rats.
Accepted on April 9, 1981
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