| The antiprogestin, mifepristone, has previously been shown to noncompetitively inhibit estrogen-induced endometrial proliferation in nonhuman primates (van Uem et al., 1989; Wolf et al., 1989b; Neulen et al., 1990; Neulen et al., 1996). For both economical and ethical reasons, we are encouraged to identify comparative laboratory rodent models which can substitute the need to use primate models. In the following study, we compared capabilities of the rat uterine weight bioassay versus a primate uterine bioassay, to identify the noncompetitive antiestrogenic/antiproliferative effects of mifepristone.;Long-term ovariectomized monkeys were exposed to exogenous 17;In the rat model, ovariectomized immature (day 20) and adult Sprague-Dawley rats were pretreated with E2 for 3 days, followed by E2 plus mifepristone (various doses) for 3 additional days. E2 replacement was either given as 0.5 ;Based on the results summarized here, we do not recommend using the rat uterine weight bioassay as a substitute model for screening antiprogestins for noncompetitive antiestrogenic/antiproliferative effects on primate uterine endometrium. |
