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PubMed1984

Antiestrogenic action of dihydrotestosterone in mouse breast. Competition with estradiol for binding to the estrogen receptor.

Feminization in men occurs when the effective ratio of androgen to estrogen is lowered. Since sufficient estrogen is produced in normal men to induce breast enlargement in the absence of adequate amounts of circulating androgens, it has been generally assumed that androgens exert an antiestrogenic action to prevent feminization in normal men. We examined the mechanisms of this effect of androgens in the mouse breast. Administration of estradiol via silastic implants to castrated virgin CBA/J female mice results in a doubling in dry weight and DNA content of the breast. The effect of estradiol can be inhibited by implantation of 17 beta-hydroxy-5 alpha-androstan-3-one (dihydrotestosterone), whereas dihydrotestosterone alone had no effect on breast growth. Estradiol administration also enhances the level of progesterone receptor in mouse breast. Within 4 d of castration, the progesterone receptor virtually disappears and estradiol treatment causes a twofold increase above the level in intact animals. Dihydrotestosterone does not compete for binding to the progesterone receptor, but it does inhibit estrogen-mediated increases of progesterone receptor content of breast tissue cytosol from both control mice and mice with X-linked testicular feminization (tfm)/Y. Since tfm/Y mice lack a functional androgen receptor, we conclude that this antiestrogenic action of androgen is not mediated by the androgen receptor. Dihydrotestosterone competes with estradiol for binding to the cytosolic estrogen receptor of mouse breast, whereas 17 beta-hydroxy-5 beta-androstan-3-one (5 beta-dihydrotestosterone) neither competes for binding nor inhibits estradiol-mediated induction of the progesterone receptor. Dihydrotestosterone also promotes the translocation of estrogen receptor from cytoplasm to nucleus; the ratio of cytoplasmic-to-nuclear receptor changes from 3:1 in the castrate to 1:2 in dihydrotestosterone-treated mice. Thus, the antiestrogenic effect of androgen in mouse breast may be the result of effects of dihydrotestosterone on the estrogen receptor. If so, dihydrotestosterone performs one of its major actions independent of the androgen receptor.

Animals↗

PubMed1978

Central control of hepatic steroid metabolism: effect of discrete hypothalamic lesions.

The effects of various hypothalamic lesions on hepatic steroid metabolism in adult rats were investigated. It was found that frontal deafferentation at the retrochiasmatic and suprachiasmatic level resulted in a complete "feminization" of hepatic steroid metabolism in male rats. Such an effect was also seen when lesions involving mainly the anterior periventricular hypothalamic area and the suprachiasmatic nucleus were performed in male rats. Midline lesions, anterior to the suprachiasmatic nucleus, on the other hand, did not result in any significant effects. A moderate degree of "feminization" was obtained after bilateral lesions involving mainly the nucleus interstitialis striae terminalis but including also parts of the anterior commissure. Small lesions in the lateral preoptic area were, however, without effect. No effects were seen of analogous lesions in female rats in any of the cases studied. The present findings suggest that a region including the anterior hypothalamic periventricular area, the suprachiasmatic nucleus and adjacent areas is involved in the control of hepatic steroid metabolism. It is postulated that the neuronal cell bodies that produce a factor with an inhibitory effect on the secretion of "feminizing factor" have their origins in this area of the hypothalamus, or, alternatively, may send axons through this area to the basal hypothalamus and thus directly or indirectly influence the anterior pituitary gland.

Afferent Pathways↗

PubMed1983

Possible role of somatostatin in the regulation of the sexually differentiated steroid metabolism and prolactin receptor in rat liver.

The regulation of the sexually differentiated metabolism of 4-[4-14C]androstene-3,17-dione and the presence of PRL receptors in rat liver were studied. Electrolytic lesions in male rats placed in a restricted area in the anterior hypothalamic periventricular area caused a feminization of hepatic steroid metabolism (i.e. increased the 5 alpha-reductase and decreased the 6 beta- and 16 alpha-hydroxylase activities) and of the levels of PRL receptors (increased binding of [125I]-labeled human PRL). After periventricular lesions, histochemical analysis revealed a decrease in somatostatin-like immunoreactive cell bodies in the periventricular area. Also the number of immunoreactive somatostatin fibers in the median eminence was dramatically reduced. Somatostatin levels in the median eminence, as measured by RIA, were reduced to approximately 2-10% of control values after periventricular lesions. Large lesions in the amygdaloid complex in male rats caused a partial feminization of hepatic steroid metabolism and PRL receptors. Passive immunization during 4 days by multiple injections of an antiserum generated against somatostatin resulted in a partial feminization of the male rat liver. When somatostatin was injected into female rats, the PRL receptors were reduced to approximately 60% of the control female receptor levels. The present study indicates that the anterior periventricular hypothalamic area is important in the control of the sexually differentiated steroid metabolism and PRL receptors in the liver and that the amygdaloid complex also may have regulatory influences on this system. A possible central neuro-endocrine mediator of these sex differences in the liver could be somatostatin or a related compound.

Androstenedione↗

PubMed1992

Amino acid substitutions in the DNA-binding domain of the human androgen receptor are a frequent cause of receptor-binding positive androgen resistance.

In some subjects with genetic and endocrine evidence of androgen resistance, no defect is demonstrable in the binding of androgen to its receptor in cultured genital skin fibroblasts. We have defined the molecular defect in the androgen receptor in four unrelated subjects in this category (termed receptor positive) with the phenotype of compete or incomplete testicular feminization. In these patients we detected amino acid substitutions in either exon 2 or exon 3, which encodes the DNA-binding domain of the androgen receptor. In one patient with incomplete testicular feminization, two separate mutations were present in exon 3. Introduction of these amino acid substitutions into the androgen receptor-coding segment leads to the expression of receptor proteins that bind ligand in a normal fashion but do not activate the transcription of the androgen-responsive mouse mammary tumor virus promoter. Mobility shift assays using androgen receptor fusion proteins produced in E. coli indicate that these mutations impair binding of the receptor to specific DNA sequences. In the subject with incomplete testicular feminization, a Ser-Gly substitution at amino acid residue 595 is able to partially restore DNA-binding activity to a mutant receptor protein that carries an Arg-Pro substitution at position 615. These findings indicate that mutations in amino acid residues crucial to the binding of the androgen receptor to target DNA sequences are a common cause of receptor-binding positive androgen resistance and that variable impairment of DNA binding can lead to distinctive phenotypes.

Adolescent↗

PubMed2005

Assessing the sensitivity of different life stages for sexual disruption in roach (Rutilus rutilus) exposed to effluents from wastewater treatment works.

Surveys of U.K. rivers have shown a high incidence of sexual disruption in populations of wild roach (Rutilus rutilus) living downstream from wastewater treatment works (WwTW), and the degree of intersex (gonads containing both male and female structural characteristics) has been correlated with the concentration of effluent in those rivers. In this study, we investigated feminized responses to two estrogenic WwTWs in roach exposed for periods during life stages of germ cell division (early life and the postspawning period). Roach were exposed as embryos from fertilization up to 300 days posthatch (dph; to include the period of gonadal sex differentiation) or as postspawning adult males, and including fish that had received previous estrogen exposure, for either 60 or 120 days when the annual event of germ cell proliferation occurs. Both effluents induced vitellogenin synthesis in both life stages studied, and the magnitude of the vitellogenic responses paralleled the effluent content of steroid estrogens. Feminization of the reproductive ducts occurred in male fish in a concentration-dependent manner when the exposure occurred during early life, but we found no effects on the reproductive ducts in adult males. Depuration studies (maintenance of fish in clean water after exposure to WwTW effluent) confirmed that the feminization of the reproductive duct was permanent. We found no evidence of ovotestis development in fish that had no previous estrogen exposure for any of the treatments. In wild adult roach that had previously received exposure to estrogen and were intersex, the degree of intersex increased during the study period, but this was not related to the immediate effluent exposure, suggesting a previously determined programming of ovotestis formation.

Animals↗

PubMed1979

Metabolic activation/deactivation reactions during perinatal development.

The role of metabolic activation/deactivation reactions during development is evaluated in relation to developmental pharmacology and toxicology. Enzyme systems evaluated include the mixed-function oxidases (aryl hydrocarbon hydroxylase and oxidative demethylation), epoxide hydration and conjugation (glutathione conjugation, sulfation, and glucuronidation). Placental transfer and milk secretion of chemicals are discussed in relation to maternal, placental, and fetal metabolism. Normal patterns of enzyme development can be modified in two ways: (1) enzyme induction and (2) enzyme imprinting. Postnatal induction of the mixed-function oxidases and glucuronyl-transferase following treatment of pregnant rats with TCDD is shown to be caused primarily by newborn exposure to TCDD in milk. Structure-activity relationship are defined for the perinatal induction of hepatic enzymes by the pure PCBs. PCBs are divided into two classes: P-450 inducers and P-448 inducers. Imprinting or programming of hepatic metabolism is a function of the sexual differentiation of enzyme activity; male and female activities are similar in prepubertal animals, whereas pronounced sex differences are evident in adults. Treatment of newborn rats (days 2--6) with diethystilbestrol or testosterone resulted in a feminization (decrease) of mixed-function oxidation and glucuronidation in adult males. No changes were seen in immature males or females or adult females. This effect appears to be irreversible and is under pituitary-hypothalamic-gonadal control. In addition to the feminization of enzyme activity, neonatal exposure to hormonally active chemicals also feminizes the hepatic response to cadmium in resultant adult animals.

Animals↗

PubMed1979

Time-studies of the changes in the sex-dependent activities of enzymes of hepatic steroid metabolism in the rat during oestrogen administration.

This investigation was undertaken to elucidate the amount of oestradiol and duration of its administration necessary to cause complete feminization of the activities of cytoplasmic 3 alpha- and 17 beta-hydroxysteroid dehydrogenase, microsomal 3 alpha- and 3 beta-hydroxysteroid dehydrogenase and microsomal 5 alpha-reductase in male rat liver. With the exception of cytoplasmic 3 alpha-hydroxysteroid dehydrogenase, 5 microgram oestradiol/d for 8 days and less was sufficient to cause complete feminization. The order of oestrogen sensitivity was cytoplasmic 3 alpha-hydroxysteroid dehydrogenase greater than microsomal 3 beta-hydroxysteroid dehydrogenase greater than microsomal 3 alpha-hydroxysteroid dehydrogenase greater than microsomal 5 alpha-reductase greater than cytoplasmic 17 beta-hydroxysteroid dehydrogenase. Although the changes occurring after oestradiol administration are qualitatively the same as after testectomy, they occur more rapidly. This rules out the possibility that oestradiol exerts its effect via androgen deprivation. Diethylstilboestrol administration causes the same changes in cytoplasmic 17 beta- and microsomal 3 beta-hydroxysteroid dehydrogenase activity as oestradiol, although the dosage must be increased 100 fold. The effect of diethylstilboestrol on 5 alpha-reductase activity changes with the dose applied. Doses up to 100 microgram/d partially feminize the activity, but at higher doses the enzyme activity is repressed.

17-Hydroxysteroid Dehydrogenases↗

PubMed2001

Use of antibodies against LH receptor, 3beta-hydroxysteroid dehydrogenase and vimentin to characterize different types of testicular tumour in dogs.

Testicular tumours in dogs are of Sertoli cell, Leydig cell or germinal origin and mixed tumours are also frequently observed. The cellular components of mixed tumours are usually identified by histological examination but sometimes this is difficult. In this study, a panel of specific antibodies was used to identify the different cell types in testicular tumours by immunohistochemistry. Leydig cells were identified using an antibody against the LH receptor and an antibody against the steroidogenic enzyme 3beta-hydroxysteroid dehydrogenase (3beta-HSD), both of which are characteristic of Leydig cells in testes. Sertoli cells were identified using an antibody against the intermediate filament vimentin. Seminoma cells did not stain with any of these antibodies. Vimentin was used only in histologically complex cases. Eighty-six tumours, diagnosed histologically as 29 Sertoli cell tumours, 25 Leydig cell tumours, 19 seminomas and 13 mixed tumours, were studied. Feminization was observed in 17 dogs. Leydig cell tumours stained positively with the antibodies against the LH receptor and 3beta-HSD, whereas seminomas and Sertoli cell tumours were negative (unstained). The antibody against vimentin stained both Sertoli and Leydig cells, and tumours arising from these cells, but not seminomas. Immunohistochemistry revealed that three tumours identified histologically as Sertoli cell tumours were actually Leydig cell tumours. In 14 dogs the histological diagnosis appeared to be incomplete, as mixed tumours instead of pure types of tumours were identified in 11 dogs, and in three dogs mixed tumours appeared to be pure types. Hence, the histological diagnosis was insufficient in approximately 20% of dogs. Furthermore, immunohistochemical analysis of testis tumours revealed that feminization occurred in dogs with Sertoli cell tumours or Leydig cell tumours and their combinations, but not in dogs with a seminoma. In conclusion, incubation with antibodies against LH receptor and 3beta-HSD proved to be a consistently reliable method for identification of Leydig cell tumours in dogs. Vimentin can be used to discriminate between Sertoli cell tumours and seminomas. Overall, this panel of antibodies can be very useful for determination of the identity of testicular tumours in which histological characterization is complicated and the pathogenesis of feminization is not clear.

3-Hydroxysteroid Dehydrogenases↗

PubMed1982

Effects of gonadal steroid hormones on the hypothalamo-pituitary-liver axis in the control of sex differences in hepatic steroid metabolism in the rat.

The site of action of gonadal hormones in the regulation of hepatic steroid metabolism was investigated by measuring the effects of (i) implantation of estradiol into the pituitary gland or anterior hypothalamus of males and (ii) subcutaneous injection of a synthetic androgen in differentiated male and female rats. The hepatic responses measured in vitro were 5 alpha-reduction, and 6 beta- and 16 alpha-hydroxylation of androstenedione. After intrapituitary or intrahypothalamic implantation of oestradiol, 5 alpha-reductase activity increased and 6 beta- and 16 alpha-hydroxylase activity decreased in males relative to the enzyme activities of cholesterol-implanted animals, indicating a feminizing effect of the oestrogen. This effect could not be accomplished by subcutaneous injection of the same oestrogen preparation. Deafferentation had no effect on hepatic steroid metabolism in females, but caused a feminization in males. In addition, subcutaneous treatment of intact females with the synthetic androgen caused masculinization of hepatic steroid metabolism, but was without effect in differentiated animals. Treatment with synthetic androgens had no effect on the hepatic steroid metabolism in differentiated male animals. Subcutaneous injection of a potent synthetic progestagen had little effect on hepatic steroid metabolism in intact females. It is concluded that oestrogen feminizes hepatic steroid metabolism by an action at the hypothalamic-pituitary level and that an intact hypothalamic-pituitary axis is required for the masculinizing action of the synthetic androgen on hepatic steroid metabolism. It is possible that the site of action of androgens is in the anterior hypothalamus or in adjacent areas of the brain.

Androstenedione↗

PubMed1995

The phytoestrogen congeners of alcoholic beverages: current status.

The idea that alcoholic beverages might contain biologically active phytoestrogenic congeners stemmed from findings of overt feminization observed in alcoholic men with alcohol-induced cirrhosis. Specifically, in addition to being hypogonadal, these chronically alcohol-abusing men with cirrhosis frequently manifest gynecomastia, palmar erythema, spider angiomata, and a female escutcheon. These physical signs of exposure to active estrogen occur in the presence of normal or only minimally elevated levels of endogenous steroid estrogens. Because levels of circulating steroid hormones failed to provide a satisfactory explanation for the feminization observed, alternate explanations were considered. If the estrogenization observed was not entirely a function of tissue expose to steroid estrogens produced endogenously, then perhaps tissues were being exposed to exogenous estrogenic substances from dietary sources. Given the degree of alcohol abuse in the population in which hypotheses for feminization were being formed, alcoholic beverages became a prime candidate as a dietary source of exogenous estrogenic substances.

Alcoholic Beverages↗

PubMed2000

[Fortune-telling and women--contemporary characteristics of fortune-telling in Japanese society].

It is a well-known fact that women almost monopolize the field of fortune-telling in the present Japanese society--fortune-tellers and their customers (or clients) are mostly women. But once we view the relationship between women and fortune-telling in a general way, we can understand that fortune-telling is not necessarily monopolized by women. In other words, if we take for granted only the relationship between the two, we will overlook some sociological questions. Close observation of the relationship in question reveals several phenomena. One of them is 'the feminization of fortune-telling'. The feminization of fortune-telling is the process by which women's interests are channeled into fortune-telling and their monopolization of it. The purpose of this paper is to focus on this phenomenon--the feminization of fortune-telling'. By focusing on this phenomenon and analyzing its process, we can understand not only some aspects of the relationship between women and fortune-telling, but also bring up other questions regarding the image of Japanese women in the modern era.

Adult↗

PubMed2001

Peptide hormones versus steroid hormones: case studies from snail and turtle populations.

The proposed mechanisms of masculinization in gastropod mollusks (imposex) and feminization in oviparous vertebrates has focused primarily on the interaction of xenobiotics with the steroid hormone system. The evidence does not support the proposed mechanism of imposex induction, inhibition of CYP 19 (aromatase), since the changes in steroid titers occur only in the later stages of imposex. In addition, the role of vertebrate sex steroid hormones is limited in gastropods. Recent evidence suggests that peptide hormones play a key role in masculinization in snails and may be a more plausible mechanism of imposex induction. Steroid hormones play a role in feminization of oviparous vertebrates. Vitellogenin (Vtg, egg yolk) induction has been used extensively as a biomarker of feminization. However, in some species of turtles there is evidence that high levels of estradiol are necessary to initially induce Vtg. Once this imprinting occurs, lower levels of estradiol can then induce high levels of Vtg. It was found that environmental levels of estradiol do not always induce Vtg in male and juvenile turtles. However, these same levels of estradiol significantly elevate female Vtg levels. Elevated female Vtg may lead to larger, but fewer, eggs, and therefore fewer offspring. However, these offspring may have better survivorship. Alternatively, elevated Vtg may lead to a larger number of smaller eggs, which have been shown to produce smaller hatchlings with reduced survival. The effects of elevate female Vtg on fitness are difficult to assess in such long-lived species.

Animals↗

PubMed2002

Preferred partner characteristics in homosexual men in relation to speculated patterns of brain differentiation.

OBJECTIVES: The current study was designed to test a neurohormonally based theory of sexual orientation and preferred partner characteristics in homosexual men. The theory holds that the brains of homosexual men are masculinized and feminized directing attraction to targets younger and more masculine than self, and the brains of homosexual adolescents are incompletely masculinized and feminized directing attraction to targets older and more masculine than self. METHODS: Ninety-six homosexual men completed questionnaires that asked them to rate morphological and behavioral characteristics associated with ethologically relevant indicators of masculinity. The participants made ratings for themselves as adolescents and adults, their current partners and idealized partners as adults, and their idealized partners as adolescents. RESULTS: Results of within-subjects multivariate analyses of variance supported most of the hypotheses. Participants as adults rated their idealized partners as more masculine than themselves and their real partners on five measures: height, weight, muscle development, facial hair, and sexuality. As adolescents they indicated a preference for males older and more masculine than self. The participants in adulthood did not show the predicted preference for partners younger than themselves. CONCLUSION: The increased ratings of sexuality for self from adolescence to adulthood support the contention that some additional masculinization of the brain may occur with aging. The increased ratings of body size for the idealized target from adolescence to adulthood keeps the target more masculine then self across developmental periods. This phenomenon is consistent with the speculated feminization of the brain at both periods and its effects on partner preferences.

Adult↗

PubMed1990

[A new space for feminine desire].

Psychoanalitical literature evolved around the idea of a space for desire structured according to the boy-mother relationship model. Is the feminine clinical approach, together with the historical contribution of feminism, discovering a new space for feminine desire? The psychotic female, for whom the role of the father has no meaning in the mother's discourse, refuses the Law as a symbol of social authority. As for the hysteric female, she does not rely on the Father as a safeguard against the emptyness that lies behind the Laws and the beliefs of men. In its own way, feminism adopts these positions of psychotic rejection and hysteric contestation by projecting them on to the social landscape. Furthermore, feminism requires new forms of social interaction that embody the esthetical space women need to experience life as full-fledged citizens.

Cultural Characteristics↗

PubMed1990

[The feminist practice].

A discussion on contemporary feminism and feminist critical practice is proposed. The most significant aspects of debate on the constitution, reproduction, opposition and resistance in feminism are exposed. The most outstanding characteristics of anglo-american and french feminism are presented. Its implications for feminist practice are considered. No definitive conclusions arise. New theories and multiple explanations are suggested as constant methods to analyze an ever changing discussion.

Female↗

PubMed1986

Effects of neonatal and adult castration on the in vitro metabolism of steroids and xenobiotics in rat liver.

Previous studies in our laboratory have shown that the sex-differentiated metabolism of 4-androstene-3,17-dione and of several other steroid hormones in adult rat liver is "feminized" following neonatal castration of male rats, due to an influence via the hypothalamo-pituitary-liver axis. The metabolism of many xenobiotics is also sex differentiated, and an important question is whether endocrine ablations might alter hepatic carcinogen metabolism in a way explaining, for example, the decreased tendency of castrated male rats [Y.C. Toh, In: Shanmagarathnam et al. (eds.), Liver Cancer, Cancer Problems in Asian Countries, Proceedings of the Second Asian Cancer Conference, pp. 167-171. Singapore: Singapore Cancer Society, 1976] to form liver tumors following 2-acetylaminofluorene treatment. The results presented in this paper clearly show that neonatal castration of male rats, much more efficiently than adult castration, feminizes the cytochrome P-450-dependent, sex-differentiated, liver microsomal formation of 7-hydroxy-2-acetylaminofluorene, 9-hydroxy-2-acetylaminofluorene, 5-hydroxy-2-acetylaminofluorene, 1-hydroxy-2-acetylaminofluorene, and N-hydroxy-2-acetylaminofluorene from 2-acetylaminofluorene as well as the total microsomal formation of benzo(a)pyrene metabolites (male greater than female). O-Deethylation of 7-ethoxyresorufin was neither sex differentiated nor affected by castration. The capacity for in vitro sulfation of N-hydroxy-2-acetylaminofluorene in the postmicrosomal supernatant, markedly sex differentiated in the rat (male greater than female), was completely feminized by neonatal but not by adult castration. The results suggest that the influence of endocrine ablations on chemical carcinogenesis in rat liver might be mediated via the hypothalamo-pituitary regulation of certain pathways of hepatic xenobiotic metabolism.

2-Acetylaminofluorene↗

PubMedDate not supplied

Meiotic prophase in the left embryonic testis of the Japanese quail (Coturnix coturnix japonica L.).

Spontaneous, transitory feminization of the left embryonic testis occurs in the majority of male Japanese quails from day 11 of incubation until the 2nd day after hatching. The feminized gonad is composed of a testicular part and of an ovarian-like cortical region, which develops outside the tunica albuginea. The cortical region contains numerous germ cells some of which enter meiosis on day 11 (i.e. at the time characteristic of female germ cells) and reach pachytene on day 14. Cortical regions are best developed on day 16 (day of hatching), but regression, accompanied by degeneration of many germ cells, begins shortly afterwards. The mechanism of feminization of the left embryonic testis is discussed.

Animals↗

PubMed1985

Hormonal and developmental regulation of expression of the hepatic microsomal steroid 16 alpha-hydroxylase cytochrome P-450 apoprotein in the rat.

The hormonal regulation of the sexually differentiated cytochrome P-450 isozyme which catalyzes 16 alpha-hydroxylation of testosterone and 4-androstene-3,17-dione in male rat liver (P-450(16) alpha) was investigated. Estradiol valerate injection of male rats caused a decrease in P-450(16) alpha levels to almost the female level, while methyltrienolone injection had the reverse effect in female animals. Hypophysectomy abolished the sex difference in P-450(16) alpha levels. Human growth hormone infusion into male rats, mimicking the female pattern of growth hormone secretion, caused a feminization of P-450(16) alpha levels. The same effect was also seen in hypophysectomized rats of both sexes. In contrast, a different administration schedule involving 12 h injections of human growth hormone, mimicking the male pattern of growth hormone secretion, caused a masculinization of P-450(16) alpha levels in hypophysectomized rats, at a daily dose which causes feminization when given by infusion. Thus, the level of expression of P-450(16) alpha in the liver is dependent on the temporal pattern of blood growth hormone levels. While infusion of rat growth hormone into male rats also feminized the P-450(16) alpha levels, infusion of ovine prolactin had no effect. Ontogenic studies showed that the developmental pattern of P-450(16) alpha expression in the liver coincided with the known pattern of development of the sexual differentiation of hepatic steroid 16 alpha-hydroxylase activity and of the diurnal pattern of growth hormone secretion.

Aging↗