Effect of 5alpha-dihydrotestosterone implants on the fertility of male rats treated with tamoxifen.

In adult male rats, tamoxifen (TAM) reduces circulating levels of luteinizing hormone (LH) and testosterone (T) with no effect on follicle-stimulating hormone (FSH) and prolactin (PRL). It reduces the male rat's ability to inseminate the female (potency), as well as its siring ability (fecundity). The objective of the present study was to test whether androgen supplementation could reverse all or some of the observed effects of TAM. To obviate the effects of estrogen, the study was designed to evaluate the beneficial or deleterious effect of 5alpha-dihydrotestosterone (DHT), a 5alpha-reduced, nonaromatizable metabolite of T, on the reproductive functions of TAM-treated adult male rats. Adult male rats received either saline or TAM (0.2 or 0.4 mg per day p.o.) for 90 days. A group of TAM-treated rats was implanted with 6 mg DHT from day 50 to day 90. A third group of untreated animals was implanted with 0-, 1-, 3-, or 6-mg DHT implants for 90 days. Mating studies were done to assess the fecundity, potency, and fertility index at the end of the treatment. Weights of testes, pituitary, and accessory sex organs were recorded, and circulating levels of LH, FSH, PRL, T, and 17-beta-estradiol were estimated. DHT did not affect the fecundity or fertility index. TAM reduced fecundity, potency, and the fertility index. DHT implants improved the fertilizing ability of the TAM-treated male rat. This study discusses and reviews the role of T and 17-beta-estradiol in sperm-fertilizing potential in light of these observations.

Assessment of bioactivity of WHO/NIH research standard for inhibin (code 86/690) using two separate pituitary cell-culture systems.

The Research Standard for inhibin, porcine (No. 86/690) distributed by the National Institute for Biological Standards and Control, U.K. for the bioassay of inhibin was tested for its bioactivity in vitro in two rat pituitary cell culture systems. The system A was obtained from pituitaries of 12 day old immature rats while system B was obtained from pituitaries of mature male rats. The inhibin preparation failed to inhibit basal secretion of FSH in the system A. Instead it stimulated the release of both LH and FSH. 1 ng LHRH induced release of LH was inhibited by 32, 80 and 43% by 0.1, 1 and 10 IU inhibin, respectively. 10 ng LHRH induced release of FSH was inhibited in a none-dose related manner and the maximum inhibition was by 10 IU inhibin (25%). The same dose of 10 IU inhibin stimulated LHRH-induced release of LH by 35%. In system B, 1, 10, 50, 100 and 200 IU inhibin suppressed basal secretion of FSH by 0, 44, 72, 70 and 48%, respectively, while LH was suppressed by 13, 24, 46, 22 and 21% respectively. The pattern of inhibition of 10 ng LHRH induced release of LH and FSH by inhibin was similar to its effect on basal secretion. A specific dose-related inhibition of FSH was not observed. Our data question the utility of the inhibin standard (86/690).