Triglyceride metabolism in thermally-feminized males of Aedes aegypti.
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After transplantation of MtT/F4 pituitary tumor cells to male rats of the Fisher strain, the masculine type of hepatic steroid metabolism was changed into a feminine pattern of enzyme activities. Liver metabolism of steroid hormones in female rats was relatively unaffected following transplantation of pituitary tumor cells. Futhermore, extract from MtT/F4 tumors and "autonomous" pituitary tissue increased the 5alpha-reductase activity of hepatoma cells in the culture (HTC cells) at subsaturation concentrations of the substrate 4-androstene-3, 17-dione by decreasing the apparent Km of the enzyme. It is concluded that the pituitary tumor (in accord with the secretion from an "autonomous" pituitary gland) secretes "feminotropin," a novel hypophyseal principle that probably is an important regulator of hepatic steriod metabolism. It is suggested that pituitary tumor tissue of the MtT/F4 type could be used as source of feminotropin in purification studies.
Gonad histological changes were examined in Japanese medaka exposed to 17beta-estradiol (E2) during early-life stages. Two experiments were conducted at different concentrations of E2 (33.5 and 140.6 ng/L, mean value of measurement) and larvae and juveniles were observed for histological changes in the gonad. Differentiation of ovary and testis in control fish was apparent 12 days post-hatch (dph). At 12 dph, normal testes were observed in male fish that had been exposed to 33.5 ng/L E2, but at 14 and 20 dph, testis-ova was recognized in male fish. Male fish exposed to 140.6 ng/L E2 had testis-ova at 12 dph and gradual transformation to ovary was observed in male fish until 20 dph. In both experiments, the ovarian tissue in testis of male fish exposed to E2 was frequently distributed along the central transverse axis of the gonad, expanding into the transverse axis. The results indicated that 17beta-estradiol can induce testis-ova in male medaka during the larval period and sex-transformation is more frequent at higher (140.6 ng/L) than lower concentrations (33.5 ng/L) of estradiol. The results also demonstrated that testis-ova first appear in the central area of the transverse axis of testis.
Two groups of Japanese medaka (Oryzias latipes) were exposed to 17beta-estradiol (E2: 150ng/L, nominal concentration) for either a short-term exposure (STE: 0-31 days after fertilization (daf); egg-larval period) or a long-term exposure period (LTE: 0-81 daf; egg-adult period) and their subsequent spawning performance was compared in terms of fecundity, spawning time, and fertility. Most genetic males were transformed to phenotypic females by E2 following both short-term and long-term exposure, but spawning performance and gonad somatic index (GSI) of sex-transformed females (XY females) following long-term exposure were lower than those of sex-transformed females following short-term exposure and those of normal females (XX) in the control group. Sex-transformed females in the STE group and normal females possessed mature ovary, whereas most of the sex-transformed females in the LTE group possessed immature ovary, with most oocytes being in the pre-vitellogenic phase. Moreover, the chromosome types of first filial generation delivered from sex-transformed female in STE group composed with 51.9% as XY, 18.5% as YY, and 29.6% as XX. From these results, it seems that exposure to E2 until the end of the larval period produces sex-transformed medaka with high reproductive ability, similar to normal females, but longer exposure to E2 may inhibit sexual maturation in the sex-transformed female.
Many chemicals introduced into the environment by humans adversely affect embryonic development and the functioning of the male reproductive system. It has been hypothesized that these developmental alterations are due to the endocrine-disruptive effects of various environmental contaminants. The endocrine system exhibits an organizational effect on the developing embryo. Thus, a disruption of the normal hormonal signals can permanently modify the organization and future function of the male reproductive system. A wide range of studies examining wildlife either in laboratories or in natural settings have documented alterations in the development of males. These studies have begun to provide the causal relationships between embryonic contaminant exposure and reproductive abnormalities that have been lacking in pure field studies of wild populations. An understanding of the developmental consequences of endocrine disruption in wildlife can lead to new indicators of exposure and a better understanding of the most sensitive life stages as well as the consequences of exposure during these periods.
Genital malformations constitute the most common birth defects in man and domestic animals and occur frequently in males since the participation of many genes is required for sex differentiation to proceed in the male direction. The precise dose, timing, and coordination needed for their expression add to the proneness of various stages in male sex differentiation to external influences. The emerging insight, through the identification of genes involved in the sex differentiation cascade, is that over 85% of sex anomalies in human and domestic animal populations are not attributable to chromosome aberrations or to mutations in a known gene. Since a majority of severely malformed individuals are incapable of reproduction, the high rates of these defects have to be results either of new mutations or of collaboration of environmental factors with genes. Increase in specific malformations in domestic animals often indicates increased concentration of liability genes brought together in the conceptus by inbreeding. However, in human populations where inbreeding is not the norm such increases may reflect environment-induced new mutations or interaction of environmental agents with hormone-sensitive genes. This review summarizes the information currently available on the genetics of major events in male sex differentiation and briefly discusses the collaborative role that environment may play in disrupting different components of this process.
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This article discusses the link between feminist theory and midwifery practice. By incorporating concepts of feminist theory within this article, it is appropriate therefore that it should be written in the first person. I hope to illustrate why feminist theory is especially relevant to midwifery education and practice, and shall briefly highlight some of the feminist ideologies which may best fit the midwifery model. I also discuss a system of nursing education based upon feminist principles and values, devised by Hedin & Donovan in 1989, and its potential for adaptation to midwifery education.
This essay explores an alternative paradigm for epidemiology, one which is explicitly informed by a feminist perspective. We intend to expand upon recent critiques and debates within the emergent fields of "critical", "popular", and "alternative" epidemiology to examine how epidemiology's conceptual models--which are meant to contribute to the prevention of social inequalities in health, but may instead reinforce social hierarchies based on gender, race, and class--constrain our understanding of health and disease. Specifically, we examine persistent antifeminist biases in contemporary epidemiological research on women's health. Issues highlighted include: problem definition and knowledge production in women's health: biological essentialization of women as reproducers; and decontextualization and depoliticization of women's health risks. As part of this critique, we include suggestions for an emancipatory epidemiology that incorporates an alternative feminist framework.
Wild carp, Cyprinus carpio, were sampled in January and March 2000 in a section of the Anoia River (NE Spain) known to be polluted by estrogenic compounds. At each sampling time, three groups were distinguished: (1) apparently normal males; (2) apparently normal females; and (3) affected fish. The latter were characterized by the simultaneous development of male and female tissue in their gonads at a macroscopical level (six out of 31 fish sampled at this particular point), or testicular atrophy (three out of 31). Plasmatic and hepatic vitellogenin (VTG) levels and plasma testosterone (T) and estradiol (E2) were measured to observe the particular estrogenic response of the affected fish. Moreover, the response in the xenobiotic metabolizing capacity in liver was tested. This involved the analysis of mixed function oxygenase (MFO) system such as: total cytochrome P450 content, NAD(P)H cytochrome c reductases and the associated CYP1A1, EROD activity. Also, glutathione S-transferase (GST) and UDP-glucuronosyltransferase (UDPGT) as detoxifying enzymes were measured. Our results showed: (1) a highly variable VTG content in all fish groups; (2) an increase in sex hormones content in March for the female group; and (3) an enhanced xenobiotics metabolism in the affected fish group, measured as total cytochrome P450, EROD activity in the January survey and cytosolic GST in March. The observed increase in VTG, sex hormones and in most of the enzymatic activities from January to March that could also be attributed to higher water temperature.
The amphipod Gammarus duebeni harbours several species of vertically transmitted microsporidian parasites. G. Duebeni were collected from 3 localities in the UK. Animals from Budle Bay, Northumberland, were infected with Octosporea effeminans, and those from Millport, Isle of Cumbrae and Fenham Flats, Northumberland were infected with microsporidia of the genus Nosema. We derived expected distributions of parasites per host embryonic cell by modelling parasite transmission as a multitype, Galton-Watson branching process. Parasite prevalence (proportion of females infected) was significantly heterogeneous among localities. Parasite burden in zygotes was much higher for females infected with Nosema than in animals infected with O. effeminans. There was no significant difference between localities in the number of Nosema in the zygotes. Comparison of models and data from 64-cell host embryos showed that the distributions of parasites per cell were consistent with the hypothesis that sorting of parasites into daughter cells is biased for at least 1 cell lineage. Host embryos infected with O. effeminans could expect to contain a growing number of parasites in each cell generation within such biased cell lineages; similar estimates for Nosema predict a decline in the number of parasites per cell within a biased lineage. We discuss the possibility that the 2 species of parasite may be employing different strategies in order to ensure transmission to the next host generation.
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