Androgen inhibition of basal and estrogen-stimulated prolactin binding in rat liver

Abstract

Estradiol (E 2 0.25 μg) administered twice a day for 7 days to rats ovariectomized 2 weeks previously caused a 4.5-fold increase in [ 125I]ovine prolactin (PRL) binding to a rat liver crude plasma membrane fraction. Testosterone (T, 500 μug) injected in combination with E 2 caused a 75% reduction in PRL binding. In male rats (both intact and castrated) injected once daily with E 2-benzoate (EB, 10 μg/100 g body wt), T-propionate (TP, 100 μg/100 g body wt.) caused a 62–73% decrease in E 2-induced binding without affecting the high levels of plasma PRL induced by EB. DHT led to a significant inhibition of PRL binding at the relatively low doses of 10 and 2.5 μg/100 g body wt. in control and E 2-treated ovariectomized rats, respectively. T was slightly less effective than DHT in reducing PRL binding. DHT was also found to be effective in reducing PRL binding to rat liver in rats hypophysectomized bearing a pituitary homotransplant, the level of binding decreasing from 10.7 ± 0.8% to 7.4 ± 0.7% ( P < 0.01) in animals injected twice a day for 7 days (100 μug/100 g body wt.). A single injection of DHT caused a 24% reduction ( P < 0.01) in PRL binding 12 h after its injection in E 2-treated animals, the stimulatory effect of the estrogen being completely inhibited within 3–5 days of DHT treatment. These data indicate that androgens can effectively reduce prolactin binding to rat liver independently of their effect on plasma PRL.