El. Zanella et al., GnRH antagonist inhibition of gonadotropin and steroid secretion in boars in vivo and steroid production in vitro, J ANIM SCI, 78(6), 2000, pp. 1591-1597
The hormone GnRH has a stimulatory effect on gonadotropin synthesis and sec
retion. The objective of the first study was to evaluate concentrations of
FSH and LH in plasma of boars after successive treatment with SB75, a GnRH
antagonist. Thirteen boars greater than 1 yr of age (eight White Composite
[WC] and five Meishan [MS]) were injected once daily with SB75 (10 mu g/kg
of body weight) for 4 d. Plasma concentrations of LH and testosterone (T) d
ecreased after 1 h from the first dose of SB75. After 12 h of treatment, LH
gradually returned to pretreatment concentrations, but T remained suppress
ed (< 2 ng/mL) until after the last injection of SB75. There was a modest,
but significant, reduction in FSH during treatment with SB75. The prolonged
inhibitory effect of SB75 on suppression of plasma T concentrations, in th
e presence of pretreatment concentrations of LH, implied direct effects of
SB75 at the testis. In the second experiment, testicular tissue from adult
boars was incubated in the presence of three doses of human chorionic gonad
otropin (hCG; 0, .5, and 5 IU) with SB75 (250 ng/mL) or with Deslorelin, a
GnRH agonist (500 ng/mL). Samples of media were collected every hour for 3
h, and concentrations of T and estrone (El) were determined by RIA. Concent
rations of T and El increased with time in response to treatment with hCG.
Co-treatment with SB75 decreased media concentrations of T (P < .01) and E1
(P < .03) compared to controls (77.9 vs 85.7 +/- 2.0 and 4.7 vs 5.3 +/- .2
ng/g). In contrast, treatment with Deslorelin had no effect on the amount
of T (P > .50) or El (P > .26) released with all dosages of hCG. These resu
lts indicate that a GnRH antagonist has a direct effect on the testis, decr
easing amounts of T and E1 released from the Leydig cells; however, treatme
nt with a GnRH agonist had no direct effect on release of these gonadal ste
roids. Thus, it remains unresolved whether the site of action of GnRH antag
onist on testicular steroidogenesis is through a testicular GnRH receptor o
r through some other mechanism.