Comparison of oestrogen and GnRH agonist analogue-induced inhibition of the pituitary-testicular function in rat

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Abstract
The purpose of the present study was to compare the inhibitory effects of estrogen and a gonadotropin releasing hormone agonist analog (GnRH-A) on the pituitary-testicular function of adult rats. Animals were treated with s.c. injections of estrogen (diethylstilbestrol, DES, 5 or 50 .mu.g/kg body wt per day) or a gonadotropin releasing hormone agonist analog [(D-Ser-(tBu)6)des-Gly10-GnRH N-ethylamide, GnRH-A, 0.4 or 4 .mu.g/kg per day] up to 12 days. Serum LH [lutropin] (24 h after the last hormone injection) decreased by 83% in 3 days with DES, but was unchanged during 12 days of GnRH-A treatment. Serum testosterone (T) decreased by 98% during DES treatment, and also clearly but less profoundly, by 89%, with GnRH-A. Maximal decrease in the weights of the ventral prostate and seminal vesicles were 73-78% with DES-treatment, but clearly slower, and to a lesser extent, with GnRH-A (33-41%). Testicular weights decreased consistently (up to 41%) with GnRH-A treatment only. DES decreased the content of testicular LH receptors by 40% in 12 days whereas GnRH-A caused a loss of 97% in LH binding. Testicular lactogen receptors decreased to similar extents (by 68-78%) with both treatments. A clear increase in serum progesterone/T ratio was observed with both types of treatment, suggesting blockade of steroidogenesis at the C21 steroid level. The antigonadal actions of estrogen in the intact animal are largely due to a decrease of circulating gonadotropin levels, and those of GnRH-A are predominantly due to Leydig cell LH-receptor down-regulation and steroidogenic lesions, induced by transiently elevated gonadotropin levels. The inhibitory effects of estrogen on testicular function appeared to be faster and more complete than those of GnRH-A in the present short-term experiments.

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