Oestrogen does not affect the restoration of spermatogenesis in the gonadotrophin-releasing hormone-immunised adult rat.
Oestrogen is a metabolite of testosterone, but its role in spermatogenesis is ill-defined. Oestrogen may exert its effects on spermatogenesis, as oestrogen receptor (ER)-beta has been localised to both germ and somatic cells. This study sought to establish whether the restoration of early germ cell numbers in spermatogenesis by high-dose exogenous testosterone was influenced by its metabolite, oestrogen. The ER antagonist (ICI 182780) was administered, at a dose known to impair oestrogen action in the male reproductive tract, during testosterone treatment of gonadotrophin-releasing hormone (GnRH)-immunised rats, and germ cell numbers were determined. GnRH-immunised adult Sprague-Dawley rats (n=7-8 per group) received two doses of testosterone, either as a Silastic implant (24 cm (T24 cm)) or an injectable ester for 10 days alone or in combination with ICI 182780 (2 mg/kg, s.c. injection daily). Control rats received vehicle alone. Testes were perfusion-fixed and germ cells were quantified by the optical disector technique. GnRH-immunisation reduced (P<0.001) both type A/ intermediate spermatogonial and type B spermatogonial/ preleptotene spermatocyte number (56% of control) and leptotene/zygotene spermatocyte number (63% of control). Pachytene spermatocyte and round spermatids were reduced to 12% and l% (P<0.01) of control respectively. Testosterone treatment did not increase type A/intermediate spermatogonial number compared with GnRH-immunised controls over the 10-day study period. Treatment with testosterone-esters increased type B spermatogonial/preleptotene spermatocytes and leptotene/zygotene spermatocyte numbers (both being ~83% of control, P<0.05), while T24 cm treatment did not significantly increase their numbers (~73% of control) compared with GnRH-immunised controls. Both treatments increased pachytene spermatocyte and round spermatid numbers to 55% and 8% of control respectively. Co-administration of ICI 182780 had no effect on any of these germ cell numbers. We conclude that oestrogen action plays no role in the short-term restoration of spermatogenesis by testosterone in the GnRH-immunised rat.
Meachem
Sarah J
SJ
Prince Henry's Institute of Medical Research Block E, Level 4, Monash Medical Centre, 246 Clayton Road, Clayton, Victoria 3168, Australia. sarah.meachem@phimr.monash.edu.au
Robertson
David M
DM
Wreford
Nigel G
NG
McLachlan
Robert I
RI
Stanton
Peter G
PG
D000818:Animals; D004958:Estradiol / Q000031:analogs & derivatives* / Q000494:pharmacology*; D004965:Estrogen Antagonists / Q000494:pharmacology*; D004967:Estrogens / Q000494:pharmacology; D005640:Follicle Stimulating Hormone / Q000494:pharmacology; D000077267:Fulvestrant; D007987:Gonadotropin-Releasing Hormone / Q000494:pharmacology*; D007114:Immunization; D007986:Luteinizing Hormone / Q000097:blood; D008297:Male; D051381:Rats; D017207:Rats, Sprague-Dawley; D013076:Sperm Count; D013087:Spermatids / Q000187:drug effects; D013090:Spermatocytes / Q000187:drug effects; D013091:Spermatogenesis / Q000187:drug effects*; D013739:Testosterone / Q000097:blood / Q000494:pharmacology
D004965:Estrogen Antagonists; D004967:Estrogens; D000077267:Fulvestrant; D007987:Gonadotropin-Releasing Hormone; D013739:Testosterone; D004958:Estradiol; D007986:Luteinizing Hormone; D005640:Follicle Stimulating Hormone