Cryptorchidism: Residual Effects on Steroid-Regulated Gonadotropin Release in Recently Castrated Rhesus Monkeys

Publisher Website
Google Scholar
Abstract
The testicular components of feedback control of gonadotropins in primates was studied in 6 cryptorchid (CO) and 3 sham-operated (control) rhesus monkeys (M. mulatta) that were castrated (day 0) 420 days after the initial operation. Gonadotropins [luteinizing hormone (LH) and follicle stimulating hormone (FSH)], testosterone (T), and estradiol-17.beta. (E2) were quantified by radioimmunoassay in serum collected daily from days 1-21, 33-40 and 48-55. Serum was collected on alternate days from day 59-97. After castration, CO and control monkeys were treated identically: T and E2 in Silastic capsule implants from day 0-58, T from day 59-80, and no treatment after day 80. Serum concentrations of T fluctuated between 5-10 ng/ml, and E2 fluctuated between 25-60 pg/ml during treatment. Each animal received a single s.c. injection of estradiol benzoate (EB), 42 .mu.g/kg body wt, on days 1-3, 16, 35 and 50, to establish the onset of positive feedback responses to estrogen with time after castration. None of the animals released LH or FSH in response to EB given on days 1-3. By day 16, all CO animals released LH and FSH in response to EB, but none of the control monkeys responded. A similar difference in LH levels between CO and control monkeys was found on day 35. On day 50 the amount of LH released in response to EB in 1 of these control animals was similar to the amount released in CO animals. Treatment with T plus E2 maintained basal LH at precastration levels for 58 days when E2 was removed. Serum LH gradually rose to postcastration levels thereafter. Baseline FSH was significantly elevated on day 16 in serum from CO animals only. Cryptorchidism in nonhuman primates affects responsiveness of the hypothalamic-pituitary axis to feedback control by steroids. The data appear relevant to the enigma of the inability of estrogen to affect gonadotropin release when the testes are present, i.e., they suggest that a substance (or substances) produced by the germinal epithelia is responsible for this blockade of estrogen action.