Variability in sperm suppression during testosterone administration to adult monkeys is related to follicle stimulating hormone suppression and not to intratesticular androgens.
Sex steroid-based male contraceptive regimens do not induce consistent azoospermia. The reason for this variable response is obscure. We used normal adult male monkeys, Macaca fascicularis (n = 9) as a model of testosterone (T)-induced gonadotropin suppression to understand the basis for variability in spermatogenic suppression during hormonal contraception. As observed in men, T administration to these monkeys induced azoospermia in some animals and variable degrees of spermatogenic suppression in others. Based on their sperm counts, we divided these animals into two groups: azoospermic (azoo; n = 4) and nonazoospermic (nonazoo; n = 5) groups. Sperm density, testis volumes, and serum T, bioassayable LH (bioLH), immunoassayable FSH (immunoFSH), bioassayable FSH (bioFSH), and inhibin B were examined every 2 wk during the control period, 20 wk of T administration using SILASTIC brand (Dow Corning Corp.) implants, and recovery. Testes were biopsied for estimation of intratesticular T, dihydrotestosterone, and 5alpha-androstane-3alpha,17beta-diol. Serum T levels increased 1.5- to 2-fold, leading to decreased bioLH levels (48% of control) and intratesticular T levels (15% of control); neither LH nor intratesticular T levels differed between the azoo and nonazoo groups. In contrast, serum levels of FSH, by both bio- and immunoassay, during T administration were significantly lower in the azoo than in the nonazoo group. These results suggest that the degree of suppression of spermatogenesis is closely related to the degree of suppression of FSH levels and not to the levels of intratesticular androgens or to serum LH. These results imply that FSH plays a key role in supporting spermatogenesis in monkeys in this experimental regimen and suggest that maximal suppression of FSH may be essential to ensure consistent azoospermia in men during hormonal contraception.
Narula
Anita
A
Population Center for Research in Reproduction, Department of Medicine, University of Washington, Seattle, WA 98195, USA.
Gu
Yi-Qun
YQ
O'Donnell
Liza
L
Stanton
Peter G
PG
Robertson
David M
DM
McLachlan
Robert I
RI
Bremner
William J
WJ
D000728:Androgens / Q000378:metabolism*; D000818:Animals; D001835:Body Weight; D005640:Follicle Stimulating Hormone / Q000037:antagonists & inhibitors* / Q000097:blood; D012739:Gonadal Steroid Hormones / Q000378:metabolism* / Q000494:pharmacology*; D007265:Inhibins / Q000097:blood; D007986:Luteinizing Hormone / Q000097:blood; D008252:Macaca fascicularis; D008297:Male; D009845:Oligospermia / Q000139:chemically induced / Q000503:physiopathology; D009929:Organ Size / Q000187:drug effects; D012016:Reference Values; D013091:Spermatogenesis / Q000187:drug effects*; D013737:Testis / Q000033:anatomy & histology; D013739:Testosterone / Q000097:blood / Q000378:metabolism* / Q000494:pharmacology*
D000728:Androgens; D012739:Gonadal Steroid Hormones; C422364:inhibin B; D013739:Testosterone; D007265:Inhibins; D007986:Luteinizing Hormone; D005640:Follicle Stimulating Hormone