We have shown previously that estradiol-17β(E2) reduces number of ovulations in cyclic rats, induces atresia of the dominant preovulatory follicle in monkeys, and that the initial effects of this treatment include reduced viability and estrogen accumulation in vitro by aspirated granulosa cells (GC) from monkeys and hamsters. The present experiment was designed to determine whether the reduction in estrogen accumulation can be ascribed to a direct action of E2on the aromatization of androgen to estrogen in vitro. Female hamsters were injected with 30 I.U. pregnant-mare serum gonadotropin i.p. and sacrificed 3 days later. GC were aspirated from the largest follicles and incubated for 48 h (“initial incubation” period) in the presence of human pituitary follicle-stimulating hormone (hFSH, 100 ng/ml). Following initial incubation, GC were further incubated for up to 24 h (“secondary incubation” period). During this subsequent incubation, medium was supplemented with 100nM3H-1β-androstenedione (3H-A4). Initial incubation with E2at doses of 10 ng/ml, 100 ng/ml and 1 μm E2/ml induced variability in GC response, and a maximal depression of ∼70. The inhibition by E2of hamster GC function in vitro parallels that shown in vivo for both hamsters and monkeys, but contrasts with that shown for rats. Thus, hamsters may represent an appropriate model in which to study the atretogenic effects of E2directly on antral follicle
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