Steroids mediate the gonadotropic stimulus of oocyte maturation in fish and amphibians. Such role of steroids in mammals has not been confirmed until recently. A series of studies presented data suggesting that steroids might be involved in meiosis of mouse oocytes. Here we examined this suggestion using in vitro cultures of rat and mouse follicle-enclosed oocytes (FEOs) and cumulus-enclosed oocytes (CEOs). In FEOs that mature only in response to gonadotropins or other stimuli we tested the ability of steroids to trigger meiosis and whether addition of steroid receptor antagonists blocks LH/hCG stimulation of meiosis. In CEOs that mature spontaneously, we tested whether steroid antagonists block maturation and whether steroids overcome the inhibition of maturation by hypoxanthine (Hx), a mild inhibitor of phosphodiesterases. The progesterone antagonists mifepristone (RU 486) and Org 31710, as well as the estrogen antagonist faslodex did not prevent LH-triggered maturation of rat or mouse FEOs or the spontaneous maturation of CEOs. In accordance, the progesterone agonist, promegestone (R5020) and estradiol did not stimulate the resumption of meiosis in rat and mouse FEOs, and both did not overcome the Hx inhibition of meiosis in rat and mouse CEOs. Flutamide, an androgen antagonist, did block meiosis in rat FEOs, but this action could not be affected by adding dihydrotestosterone (DHT), suggesting that it was not androgen receptor mediated. Flutamide did not affect spontaneous maturation of rat CEOs and DHT could not stimulate meiosis inhibited by Hx. Thus, in contrast to lower vertebrates, in mammals steroids do not seem to serve as an obligatory signal by which the somatic cells of the follicle transfer the gonadotropic stimulation of meiosis to the oocyte.