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O ocyte maturation in lower vertebrates is triggered by maturation-inducing hormone (MIH), which acts on receptors located on the oocyte membrane and induces the activation of maturation-promoting factor in the oocyte cytoplasm (1-4). During the course of maturation, oocytes undergo drastic morphological changes associated with progression of the meiotic cell cycle, in which breakdown of the oocyte nuclear envelope [germinal vesicle breakdown (GVBD)] occurring at the prophase͞metaphase transition is usually regarded as a hallmark of the progress of oocyte maturation. Two MIHs, 17␣,20␤-dihydroxy-4-pregnen-3-one (17,20␤-DHP) and 17␣,20␤,21-trihydroxy-4-pregnen-3-one (20␤-S), have been identified in several fish species (5, 6). In goldfish, 17,20␤-DHP has been shown to induce oocyte maturation by stimulating the de novo synthesis of cyclin B, a regulatory subunit of maturationpromoting factor (7). Although progestins including 17,20␤-DHP and 20␤-S are the most potent steroid inducers of oocyte maturation in fish, other hormones such as deoxycorticosterone and testosterone, but not estradiol or its analogs, are also effective (8).Several endocrine-disrupting chemicals, Kepon and dichlorodiphenyldichloroethane, have been reported to antagonize MIH-induced meiotic maturation of fish oocytes in vitro (9). One of the environmental endocrine-disrupting chemicals (EEDCs), diethylstilbestrol (DES) is a nonsteroidal substance that was prescribed from the late 1940s to the early 1970s to pregnant women to prevent abortion, preeclampsia, and other complications of pregnancy. Male and female offspring exposed in utero to DES may develop multiple and neoplastic lesions of the reproductive tract, along with other changes, during development (10). Here we show that exposing fish oocytes to DES at a dose within a range similar to that used in experimental exposure to 17,20␤-DHP induces oocyte maturation. Estradiol-17␤ has been reported to be ineffective in inducing fish oocyte maturation (11, 12) and even inhibitory in several teleost species (13-15). Thus, the stimulatory effect of DES to induce fish oocyte maturation observed in this study has not been published previously. This report shows that EEDC can potentially induce oocyte maturation like an endogenous MIH, 17,20␤-DHP. Materials and MethodsMaterials. Goldfish were purchased from a local supplier and maintained at 15°C until used. Zebrafish were maintained at 28.5°C on a 14-h light͞10-h dark cycle (16). 17,20␤-DHP, DES, DES dimethyl ether (DM-DES), DES dipropionate (DP-DES), and 17␤-estradiol were purchased from Sigma. Dimethylstilbestrol (DMS) was a generous gift from J. Katzenellenbogen (University of Illinois, Urbana). 17␣-Estradiol, ethynylestradiol, butyl benzyl phthalate, di(2-ethylhexyl)-phthalate, and pentachlorophenol were obtained from Wako Pure Chemical (Osaka). Other chemicals were purchased as follows: hexestrol (HEX; ICN); trans,trans-dienestrol(␣-dienestrol) (DIES; U.S. Pharmacopeia, Rockville, MD); resveratorol (Calbiochem); DDTs (AccuStandard, New Haven, ...

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Development of desmin-positive hepatic stellate cells was studied in mice using double immunofluorescent techniques and in vitro cultures with special attention given to their cell lineages. Several studies recently reported on the presence of cells that are immunologically reactive with both antidesmin and anticytokeratin antibodies in young fetal rat livers, and suggested the possibility that these cells give rise to hepatocytes and hepatic stellate cells. At early stages of mouse liver development, stellate cells with desmin-positive filaments were scattered in the liver parenchyma. However, the stellate cells definitely differed from hepatoblasts and hepatocytes in terms of their morphology and expression of desmin and hepatoblast and hepatocyte-specific E-cadherin in the liver. Fetal hepatoblasts and hepatocytes did not react with antidesmin antibodies, nor did desmin-positive stellate cells express E-cadherin in vivo and in vitro. Thus it is likely that desmin-positive stellate cells and hepatoblasts belong to different cell lineages. In the fetal liver, the desmin-positive stellate cells surrounded blood vessels, and extended their processes to haematopoietic cells and megakaryocytes. Many, but not all, hepatoblasts and hepatocytes were observed to be associated with the stellate cells. At fetal stages, cellular processes positive for desmin in the stellate cells were also thick compared with those in the adult liver, in which desmin-positive stellate cells lay in Disse's space and were closely associated with all hepatocytes. These developmental changes in the geography of desmin-positive cells in the liver parenchyma and their morphology may be associated with their maturation and interactions with other cell types.