Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Feminization”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,477 records · Page 82Linked to original sources
PubMed1988

Pretreatment of chick embryos with estrogen in ovo prevents mullerian duct regression in organ culture.

Diethylstilbestrol (DES) feminizes chick embryos in ovo, preventing regression of the Mullerian ducts (MDs). The feminized testis, however, despite its ovarian-like appearance, continues to produce Mullerian inhibiting substance (MIS). This study was designed to test whether exogenous DES preserved the MD against endogenous MIS by affecting the target organ (feminization). DES (0.1 mg) was injected into the air sacs of 5-day-old chick embryos. Testes were obtained from 15-day-old chick embryos and MDs from 8-day-old chick embryos and combined in organ culture for 72 h. MD regression was examined macroscopically and microscopically after 3 days in vitro in medium without DES (group A: n = 155) and with 10(-6) M DES (group B: n = 169). Four types of coculture were set up as follows: 1) Control testis with control MD; 2) DES-treated testis with DES-treated MD; 3) Control testis with DES-treated MD; 4) DES-treated testis with control MD. In medium without DES (group A), MD regression was inhibited significantly when the duct was pretreated with DES [2) and 3) vs. 1) and 4)]. The pretreated testis produced slightly less regression [4) vs. 1)], but this was not significant. Previous studies in ovo had suggested that estrogen prevented MD regression directly as well as causing feminization of the testis, because MIS secretion was not inhibited from the feminized gonad. These results show that pretreatment of the MD with DES blocks regression in vitro by a normal testis, confirming that the primary site of action of estrogen is on the duct itself.

Animals↗
PubMed1992

Comparison of the effects of the 5 alpha-reductase inhibitor finasteride and the antiandrogen flutamide on prostate and genital differentiation: dose-response studies.

Studies were performed to compare the effects of 5 alpha-reductase inhibition and antiandrogen receptor blockade on differentiation of male internal and external genital structures and prostate in the rat. Dose-response studies were performed on male rats treated in utero during the period of sexual differentiation with either the potent 5 alpha-reductase inhibitor finasteride or the antiandrogen flutamide. The treated animals were raised to adulthood and killed, and genital structures were evaluated. Treatment with the 5 alpha-reductase inhibitor finasteride at a dose of 25 mg/kg.day resulted in significant feminization of the external genitalia. There was no further feminization of the genitalia at doses up to 300 mg/kg.day. Wolffian ductal differentiation occurred at all doses evaluated. Seminal vesicle weight, however, significantly decreased at 25 mg/kg.day, but without a further decrease at higher doses of the 5 alpha-reductase inhibitor. Vas deferens and epididymal weights were unchanged at all doses evaluated. There was a significant decrease in prostate size at 25 and 50 mg/kg.day, with no further decrease at higher doses. In flutamide-treated animals, complete feminization of the genitalia occurred at 24 mg/kg.day in all animals. At 18 mg/kg.day, Wolffian ductal differentiation occurred, but seminal vesicle weight was decreased. At dosages of 100, 200, and 300 mg/kg.day flutamide, the vas deferens was absent unilaterally or bilaterally, with small remnants of epididymal head and tail present. At dosages of 24 mg/kg.day and above, the prostate was absent. Studies with the 5 alpha-reductase inhibitor finasteride demonstrate the dependency of prostate and male external genital differentiation on dihydrotestosterone (DHT). However, unlike androgen receptor blockade with flutamide, finasteride did not totally abolish prostate differentiation or completely feminize the external genitalia, despite increasingly higher doses. Since there is no evidence of multiple 5 alpha-reductase isoenzymes to date in the rat, these results suggest that testosterone (T) can compensate for DHT to some degree at the level of the androgen receptor. Wolffian differentiation, however, was not affected by inhibition of DHT, demonstrating its T dependency, but seminal vesicle growth was impaired. Thus, inhibition of 5 alpha-reductase activity limits seminal growth potential in adulthood. Studies with the antiandrogen flutamide show that at doses significantly above that required to completely block prostate differentiation and cause genital feminization, Wolffian ductal differentiation is significantly impaired. Thus, higher doses of flutamide are needed to block the paracrine effect of T on the Wolffian ducts.

5-alpha Reductase Inhibitors↗
PubMed1975

Laparoscopy in endocrine and genetic disorders of the gonads.

The guideline of this work is to examine the diagnostic value of laparoscopy in some endocrine and genetic syndromes connected with gonadal pathology or abnormal sexual development in relation to the various hormonal and cytogenetic techniques usually utilized by the endocrinologist. After a brief introduction, Chapter 1 stresses our purpose to examine the advantages and limits of laparoscopy by investigating the most significant cases that came to our observation. Attention is drawn in Chapter 2 to the application of laparoscopy in a particular form of amenorrhea (uterus absence), admittedly of great endocrinologic interest. In particular, the results obtained by the application of this technique are reported in cases of uterus agenesis and the testicular feminization syndrome. The clinical, cytogenetic and hormonologic study of one case of uterus agenesis is reported together with that of four cases of the testicular feminization syndrome with the view to discussing the differential diagnosis between these two syndromes and the particular diagnostic problems connected with the latter. Our conclusion is that laparoscopy, although usually having only a confirmatory value in these syndromes, may assume in certain cases major diagnostic importance (the post-puberal testicular feminization syndrome without palpable gonads, the pre-puberal testicular feminization syndrome, rare cases of the testicular feminization syndrome associated with chromosome aberrations). Chapter 3 discusses the application of laparoscopy in female gonadal dysgenesis on the basis of three cases of Turner's syndrome with different diagnostic problems and one of pure gonadal dysgenesis. It is stressed that, although in the majority of cases of Turner's syndrome the laparoscopic findings are quite characteristic (streak gonads), in some cases the gonads may also present the aspect of hypoplastic ovaries. This finding is observed in two cases of Turner's syndrome with XO/XX mosaicism, of which one case with spontaneous menarche. The diagnostic value of laparoscopy is discussed in the cases of pure gonadal dysgenesis and in variants of Turner's syndrome chromatin-positive with X chromosome partial monosomy and chromatin-negative with a Y chromosome. Our conclusion is that laparoscopy assumes particular diagnostic value in cases of pure gonadal dysgenesis without chromosome aberrations, because chromosome aberrations may be absent in this syndrome, as well as in chromatin-negative variants with a Y chromosome because the gonads and gonaducts differentiation may be variable.

Adolescent↗
PubMed1996

[Testicular tumors in dogs: a literature review].

The incidence of testicular tumours in dogs is higher than in other species. The main three types are: Sertoli cell tumour, seminoma, and Leydig cell tumour. Metastases are rare. Sertoli cell tumours, and to a lesser extent Leydig cell tumours, are often associated with feminization, which occurs in 19% and 5% of cases, respectively. Seminomas are rarely associated with feminization. Feminization seems to be the result of an excessive oestrogen production by the tumour. In severe cases this may lead to bone marrow depression. Atrophy of the contralateral testis is a common finding. It is not clear whether this is a result of feminization or of age because most tumours occur in older dogs. By investigating the morphology of the testis, and the endocrinological and fertility status of the dog this phenomena is hopefully going to be explained. Extra attention is given to the pathogenesis of feminization.

Androgen-Insensitivity Syndrome↗
PubMed1995

Hypogonadism is not related to the etiology of liver cirrhosis.

We investigated the clinical and laboratory findings of hypogonadism and feminization in male patients with viral or alcoholic cirrhosis to determine whether chronic liver disease plays a primary role in the development of sexual dysfunction and hormonal changes. Two groups of male patients with liver cirrhosis (23 alcoholic, 33 viral) age- and Child's grade-matched, and 20 age-matched healthy men, as a control group, were included in this study. Clinical signs of hypogonadism and feminization were examined in the cirrhotic patients. Follicle-stimulating hormone, luteinizing hormone, prolactin, testosterone, free testosterone, estradiol, androstenedione, dehydroepiandrosterone sulfate, and sex hormone-binding globulin were estimated in all groups. Seminal fluid was also analyzed in 7 alcoholic and 15 viral cirrhotics. Serum levels of estradiol, androstenedione, and sex hormone-binding globulin were significantly higher, and free testosterone and dehydroepiandrosterone sulfate levels were significantly lower in both groups of cirrhotics compared with the control group. Child's C patients in both groups of cirrhotics were found to have higher estradiol and lower free testosterone levels than child's A and B patients. Alcoholic and viral cirrhotics had markedly reduced sperm motility and density. The differences between alcoholic and viral cirrhotic patients in the clinical signs of hypogonadism, serum levels of sex steroids, and the results of seminal fluid analysis were not statistically significant. These findings suggest that liver cirrhosis per se, independent of etiology, causes hypogonadism and feminization, and that the degree of hypogonadism and feminization correlates well with the severity of liver failure.

Adult↗
PubMed2007

Black and White women's perspectives on femininity.

The authors explore how Black and White women view three aspects of normative femininity, and whether self-rated femininity is related to feminism. Through telephone surveys, a nationally representative sample of women (N=1130) rated themselves on feminism and items derived from Collins' (2004) benchmarks of femininity: feminine appearance, traits, and traditional gender role ideology. Confirmatory factor analysis revealed both groups conceptualized femininity as including the same dimensions, although Black women rated themselves higher on items related to feminine appearance. Among White women, traditional gender ideology was negatively related to feminism; among Black women, wearing feminine clothes was positively related to feminism. Results are discussed in terms of possibilities for resistance to the hegemonic concept of femininity that both groups share.

Adolescent↗
PubMed1982

Digoxin does not alter plasma steroid levels in health men.

Digoxin has been reported to induce feminizing effects in man. It does not compete for estradiol cytosol receptors in human breast carcinoma cells, however, and has no uterotrophic effect. We therefore investigated whether feminization might be due to digoxin action on plasma concentrations of sex steroids. Six healthy men (31.5 +/- 4 yr old) received therapeutic doses of digoxin for 43 days. We measured plasma concentrations of testosterone, androstenedione, dehydroepiandrosterone, estrone, estradiol, progesterone, 17-hydroxyprogesterone, cortisol, and aldosterone. During 35 days on digoxin levels of these steroids remained in the normal range and there was no change from before-drug values. Digoxin was in the therapeutic range of 1.9 +/- 3 nmol/l throughout. After stimulation by adrenocorticotropic hormone or human choriongonadotropin, the rise in plasma steroids was in the same range as when digoxin was given, as well as 16 wk after it had been discontinued. A normal rise in luteinizing hormone after luteinizing hormone-releasing hormone showed that the hypothalamogonadal feedback was not altered by digoxin. Free testosterone, estradiol, and cortisol concentrations under basal conditions and after stimulation were also the same before and after drug. It is concluded that the estrogen-like activity of digoxin cannot be explained by altered steroid availability from plasma. Feminizing effects attributed to digoxin may be caused by other conditions known to influence sex steroid hormones that are common in patients with heart disease. Our data suggest that digoxin may be the preferred digitalis therapy to avoid feminizing effects.

Adrenal Cortex Hormones↗
PubMed1980

Cytochemical correlates of structural sexual dimorphism in glandular tissues of the mouse.

Circulating androgens are known to effect a sexual dimorphism of the submandibular gland and kidney of the mouse. Enzyme histocytochemical differences that correlate with these structural changes have been the subject of much study, especially in the kidney. In the present study, emphasis was placed on the hypogonadic effects of diabetes mellitus on the submandibular gland and kidney of C57Bl/KsJ db/db inbred mice with an autosomal recessive disease resembling maturity onset human diabetes mellitus. These glands of adult diabetic mice of both sexes were compared with those of unafflicted heterozygous littermates. The mitochondrial cytochrome oxidase and peroxisomal and cytoplasmic catalase were studied in their submandibular glands and kidneys. The parasympathetic innervation of the submandibular glands was studied by a histochemical method for acetylcholinesterase. The extensive differentiation of striated ducts of the submandibular gland into granular tubules in the postpubertal male mouse was readily evident with the cytochrome oxidase procedure. This differentiation resulted in ductal staining patterns characteristic of the sexes. Alteration of these patterns suggested that demasculinization or feminization was occuring in the male diabetic mice and that masculinization or virilization (defeminization) was occurring in the female diabetics. Similarly, in kidney, study of the parietal epithelium of Bowman's capsule revealed feminization in the male diabetics and masculinization in the female diabetics. With the catalase procedure, a dramatic sexual dimorphism was observed in the kidneys of the heterozygous unafflicted mice. Peroxisomal staining of epithelial cells of the proximal convoluted tubules was much more intense in the outer medulla of the male than of the female. In kidneys of the diabetics, the staining patterns again suggested that feminization of the male and masculinization of the female kidneys had occurred. On the other hand, neither a sexual dichotomy nor effects due to diabetes could be observed in the characteristic catalase staining observed in the luminal epithelial cells of submandibular gland distal ducts. The parasympathetic innervation of the submandibular gland, as revealed by the acetylcholinesterase method, was also markedly sexually dimorphic in the unafflicted mice. This was due to the more extensive innervation of the larger granular ducts characteristic of male than of the smaller striated ducts of the female. As a result of diabetes, the innervation and duct size decreased in the submandibular gland of the male, suggesting feminization, whereas they increased in the female suggesting masculinization. These changes were consistent with those observed in sumandibular gland with the cytochrome oxidase procedure. Attempts were made to interrelate all of the enzyme histochemical changes observed in submandibular gland and kidney with the weights of these glands, sex, gonadal weights, diabetic status and urinary protein excretion...

Acetylcholinesterase↗
PubMed1975

Developmental effects of neonatal sex hormones on spatial and activity skills in the white rat.

The purpose of this experiment is to extend these experiments by using varying neonatal hormonal differentiation processes and to examine the effects of these different methods of neonatal feminization on changes in spatial and activity skills. The experiment involved three neonatally feminized groups of male rats: 'castration alone', 'estrogen alone', and 'estrogen injected castrates' together with one female sample, 'testosterone injected castrates', while treated and untreated male and female controls were also used. The data provide partial support for the major hypotheses that neonatal gonadectomy and opposite sex hormones administered to male and female castrated rats (together and independently for males) would reverse the normal sex-associated abilities of the white rate (higher male spatial learning and higher female activity). However, the feminization effect for the male 'estrogen alone' and 'castration alone' experimental groups was much greater than for the male estrogen injected castrates. The masculinized females, testosterone injected castrates, also had higher spatial learning and lower activity levels, while the feminized male's spatial and activity skills were also reversed. This confirmed in part the extent to which neonatal gonadal sex hormones are effective at critical periods of development in programming the brain in terms of sex-associated spatial and activity skills. Adult hormonal replacement therapy was also administered at 12 months and supported the hypothesis that sex hormones in adults would be mainly activational and have less marked effects than the significant directional changes obtained by these neonatal sex hormones and castration techniques.

Age Factors↗
PubMed2005

Neuroprotective effects of an estratriene analog are estrogen receptor independent in vitro and in vivo.

Estrogens are potent neuroprotectants both in vitro and in vivo. In the present study, we compared the potency and efficacy of a non-feminizing estrogen, 2-(1-adamantyl)-4-methylestrone (ZYC-26), with its parent estrogen, estrone, and an expected non-neuroprotective 3-O-methyl analog of (17beta)-2-(1-adamantyl)estradiol (ZYC-23). These estratriene derivatives were tested for their ability to protect in an in vitro lipid peroxidation model, to neuroprotect against oxidative stress in cell culture models, to bind the estrogen receptors (ERalpha and ERbeta), to elicit uterotrophic effects, and to affect brain damage from transient middle cerebral artery occlusion. We observed that in contrast to estrone, neither ZYC-26 nor ZYC-23 bound to either estrogen receptors (ER) and both failed to elicit a uterotrophic response. In vitro, the active estrogen analogue ZYC-26 was more potent that estrogen in its ability to inhibit lipid peroxidation and to protect HT-22 cells from either glutamate or iodoacetic acid (IAA) toxicity. Further, ZYC-26 was as active in preventing brain damage from transient middle cerebral artery occlusion (MCAO) as was estrone. Collectively, these studies suggest that the antioxidant activity, rather than ER binding of non-feminizing estrogens such as ZYC-26, mediates their potent neuroprotective activity. Further, in view of the now known toxicities of chronic feminizing estrogen use in older women, non-feminizing estrogens may be a useful alternative for estrogen-induced brain protection.

Animals↗
PubMed2001

Wolbachia endosymbiont responsible for cytoplasmic incompatibility in a terrestrial crustacean: effects in natural and foreign hosts.

Wolbachia bacteria are vertically transmitted endosymbionts that disturb the reproduction of many arthropods thereby enhancing their spread in host populations. Wolbachia are often responsible for changes of sex ratios in terrestrial isopods, a result of the feminization of genotypic males. Here we found that the Wolbachia hosted by Cylisticus convexus (wCc) caused unidirectional cytoplasmic incompatibility (CI), an effect commonly found in insects. To understand the diversity of Wolbachia-induced effects in isopods, wCc were experimentally transferred in a novel isopod host, Armadillidium vulgare. wCc conserved the ability to induce CI. However, Wolbachia were not transmitted to the eggs, so the capacity to restore the compatibility in crosses involving two transinfected individuals was lost. The feminizing Wolbachia hosted by A. vulgare was unable to rescue CI induced by wCc. These results showed that Wolbachia in isopods did not evolved broadly to induce feminization, and that CI and the feminizing effect are probably due to different mechanisms. In addition, wCc reduces the mating capacity of infected C. convexus males, suggesting that the bacteria might alter reproductive behaviour. The maintenance of wCc in host populations is discussed.

Animals↗
PubMed2002

Neuroendocrine control of a sexually dimorphic behavior by a few neurons of the pars intercerebralis in Drosophila.

In Drosophila, locomotor activity is sexually dimorphic and the brain area controlling this dimorphism has been mapped. The neurons of the pars intercerebralis (PI) have been suggested to participate in such differences between males and females. However, the precise physical nature of the dimorphism, the identity of the PI neurons involved, and the nature of the neuronal signal coding the dimorphism remain unknown. In this study, we used a video-tracking paradigm to characterize further the pattern of locomotor activity in Drosophila. We show that the number of activity/inactivity periods (start/stop bouts) is also sexually dimorphic, and that it can be genetically feminized in males. Moreover, the transplantation of PI neurons from a female, or of feminized PI neurons from a donor male into a receiver wild-type male is sufficient to induce the feminization of locomotor behavior, confirming that this tiny cluster of approximately 10 neurons is directly responsible for the sexual dimorphism in locomotor activity. Finally, feeding males with fluvastatin, a juvenile hormone (JH) inhibitor, also led to start/stop feminization, and this effect is reversible by the simultaneous application of methoprene, a JH analog, suggesting the existence of a neuroendocrine control, by JH, of such behavioral dimorphism.

Animals↗
PubMed1989

Analysis of the role of tra-1 in germline sex determination in the nematode Caenorhabditis elegans.

In wild-type Caenorhabditis elegans there are two sexes, self-fertilizing hermaphrodites (XX) and males (XO). To investigate the role of tra-1 in controlling sex determination in germline tissue, we have examined germline phenotypes of nine tra-1 loss-of-function (lf) mutations. Previous work has shown that tra-1 is needed for female somatic development as the nongonadal soma of tra-1(lf) XX mutants is masculinized. In contrast, the germline of tra-1(lf) XX and XO animals is often feminized; a brief period of spermatogenesis is followed by oogenesis, rather than the continuous spermatogenesis observed in wild-type males. In addition, abnormal gonadal (germ line and somatic gonad) phenotypes are observed which may reflect defects in development or function of somatic gonad regulatory cells. Analysis of germline feminization and abnormal gonadal phenotypes of the various mutations alone or in trans to a deficiency reveals that they cannot be ordered in an allelic series and they do not converge to a single phenotypic endpoint. These observations lead to the suggestion that tra-1 may produce multiple products and/or is autoregulated. One interpretation of the germline feminization is that tra-1(+) is necessary for continued specification of spermatogenesis in males. We also report the isolation and characterization of tra-1 gain-of-function (gf) mutations with novel phenotypes. These include temperature sensitive, recessive germline feminization, and partial somatic loss-of-function phenotypes.

Alleles↗
PubMed1972

Metabolism of testosterone- 14 C by cultured human cells.

The metabolism of (14)C-labeled testosterone by cultured human fibroblasts and amniotic fluid cells was investigated. Radiolabeled testosterone was incubated with the cultured cells for 48 hr, and the labeled metabolites present in the medium were subsequently identified. The major metabolic products of testosterone formed by cultured fibroblasts were Delta(4)-androstenedione, dihydrotestosterone, androsterone, and androstanediol. The amount of testosterone metabolized through each of two pathways was calculated and used to form a ratio designated the 17beta-hydroxyl/17-ketonic ratio. Fibroblasts from normal male and female children and adult females had high 17beta-hydroxyl/17-ketonic ratios indicating testosterone metabolism occurred primarily through the 17beta-hydroxyl pathway. There was change in the pattern of testosterone metabolism with age in males, i.e., adult males had much lower 17beta-hydroxyl/17-ketonic ratios than did male children. The testosterone metabolism of fibroblast cultures derived from three children with testicular feminization and their mothers was compared to normal age and sexmatched controls. Fibroblasts of children with testicular feminization metabolized testosterone predominantly through the 17-ketonic pathway and manifested a pattern of testosterone metabolism distinctly different from their sex and age matched controls. The mothers of children with testicular feminization could be distinguished from normal females by their much lower 17beta-hydroxyl/17-ketonic ratios. The much lower amounts of dihydrotestosterone and androstanediol produced by fibroblasts from patients with testicular feminization as compared with normals suggests there is a decrease in testosterone 5alpha-reductase activity in these patients. Cultured amniotic fluid cells metabolized testosterone to the same four major metabolites found in fibroblast cultures, but their activity was much lower than that of fibroblasts. Most of the amniotic fluid cell cultures metabolized testosterone largely through the 17beta-hydroxyl pathway as did fibroblasts from normal children.

17-Ketosteroids↗
PubMed2001

17beta-estradiol treatment decreases steroidogenic enzyme messenger ribonucleic acid levels in the rainbow trout testis.

In fish, estrogens are well known for their involvement in ovarian differentiation and have been shown to be very potent feminizing agents when administrated in vivo during early development. However, the mechanism of action of exogenous estrogens is poorly understood. We report here on the feminizing effects of estrogen treatment on the testicular levels of some steroidogenic enzyme messenger RNAs [mRNAs; cholesterol side-chain cleavage (P450scc), 17-hydroxylase/lyase (P450c17), 3beta-hydroxysteroid dehydrogenase (3betaHSD), 11beta-hydroxylase (P45011beta), and aromatase (P450aro)] in the rainbow trout, Oncorhynchus mykiss. Treatment was carried out by dietary administration of 17beta-estradiol (E(2); dosage of 20 mg/kg diet) to a genetically all male population. Steroidogenesis in the differentiating testis was demonstrated to be strongly altered by E(2), as this treatment resulted in considerable decrease in P450c17, 3betaHSD, and P45011beta mRNAs after only 10 days of treatment. In contrast, P450scc and P450aro mRNA levels were unaffected by E(2), with P450scc mRNA levels remaining unaltered and P450aro not stimulated by this feminizing estrogen treatment. To better characterize this E(2) effect, the same treatment was applied on postdifferentiating males, and roughly the same expression pattern was detected with a considerable decrease in testicular P450c17, 3betaHSD, and P45011beta mRNAs and a significant, but reduced, decrease in P450scc mRNA. In the interrenal, these steroidogenic enzyme mRNAs were not significantly affected by this E(2) treatment, except for a slight, but significant, decrease in P450scc mRNA. These results clearly demonstrate that estrogens have profound effects on testicular steroidogenesis and that they are acting specifically on the testis by decreasing mRNA steady state levels of many steroidogenic enzyme genes. The decrease in P45011beta mRNA, and thus inhibition of the synthesis of testicular 11-oxygenated androgens, may be an important step required for the active feminization of these genetic males.

3-Hydroxysteroid Dehydrogenases↗
PubMed2000

Sex-typicality and attractiveness: are supermale and superfemale faces super-attractive?

Many animals find extreme versions of secondary sexual characteristics attractive, and such preferences can enhance reproductive success (Andersson, 1994). We hypothesized, therefore, that extreme versions of sex-typical traits may be attractive in human faces. We created supermale and superfemale faces by exaggerating all spatial differences between an average male and an average female face. In Expt 1 the male average was preferred to a supermale (50% exaggeration of differences from the female average). There was no clear preference for the female average or the superfemale (50% exaggeration). In Expt 2, participants chose the most attractive face from sets of images containing feminized as well as masculinized images for each sex, and spanning a wider range of exaggeration levels than in Expt 1. Chinese sets were also shown, to see whether similar preferences would occur for a less familiar race (participants were Caucasian). The most attractive female image was significantly feminized for faces of both races. However, the most attractive male image for both races was also significantly feminized. These results indicate that feminization, rather than sex exaggeration per se, is attractive in human faces, and they corroborate similar findings by Perrett et al. (1998).

Adolescent↗
PubMed1998

Androgens and masculinization of genitalia in the spotted hyaena (Crocuta crocuta). 2. Effects of prenatal anti-androgens.

Pregnant spotted hyaenas were treated with anti-androgens to interfere with the unusually masculine 'phallic' development that characterizes females of this species. The effects on genital morphology and plasma androgen concentrations of infants were studied during the first 6 months of life. Although there were consistent 'feminizing' effects of prenatal anti-androgen treatment on genital morphology in both sexes, such exposure did not produce males with extreme hypospadia, as it does in other species, nor did it produce females with a 'typical' mammalian clitoris and external vagina. 'Feminization' of males resulted in a penis with the morphological features of the hyaena clitoris, and 'feminization' of females exaggerated the sex differences that are typical of this species. The effects of treatment were present at birth and persisted for at least 6 months. Treatment of pregnant females with flutamide and finasteride also markedly reduced circulating concentrations of testosterone and dihydrotestosterone in maternal plasma during pregnancy. Plasma delta 4-androstenedione was reduced in the female, but not the male, infants of treated mothers, consistent with an epigenetic hypothesis previously advanced to explain hormonal 'masculinization' of females. The present 'feminizing' effects of prenatal anti-androgen treatment are consistent with contemporary understanding of sexual differentiation, which accounts for morphological variation between the sexes in terms of steroids. However, current theory does not account for the basic genital structure of females and the present data suggest that development of the male penis and scrotum, and the female clitoris and pseudoscrotum, in spotted hyaenas may involve both androgen-dependent and androgen-independent components.

5-alpha Reductase Inhibitors↗
PubMed2003

Study of estrogenic effects on carp (Cyprinus carpio) exposed to sewage treatment plant effluents.

To investigate whether male carp (Cyprinus carpio) are really feminized by estrogen-like substances in effluent from sewage treatment plants (STPs) in Japan, exposure tests were performed using carp in water tanks that were receiving effluent from a STP. During eight weeks of exposure, we had measured their serum vitellogenin (VTG), a precursor of yolk protein specific for females that is synthesized in their liver by estrogen-like substances and that is, therefore, a biomarker of feminization. For this research, a STP with representative effluent estrogenic activity level was selected. In the first run of the tests that launched in the early spring of 2000, male carp were exposed. Results showed that the VTG concentration in male carp exposed to the effluent increased with time, while it was reduced after exposure to the effluents was stopped and the exposure was changed to dechlorinated tap water. On the other hand, in the control experiment, VTG was not detected in male carp exposed to dechlorinated tap water. Therefore, male carp might be reversibly feminized by the STP effluent. To assure whether the feminization of male carp was caused by the STP effluent at any time, two more runs of the test were performed in the summer of 2000 and February to April of 2001. However, significant level of VTG in male carp could not be observed for eight weeks. The estrogenic activities in the effluents were almost the same level throughout the tests; therefore the seasonal timing of exposure might be important for understanding this inconsistent phenomenon.

Animals↗