Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0042755 (masculinization)
 2,562 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The ovarian-peripheral gradients of various delta4 and delta5 steroids were determined for a patient with virilizing arrhenoblastoma. The high peripheral testosterone level accompanying this tumor results from increased precursor supply from both the delta4 and delta5 pathways, with the delta5 pathway predominating, and from negligible aromatase activity. A review of 45 cases of androgen-producing ovarian tumors with measurement of peripheral venous testosterone, and of 24 cases with measurement of ovarian venous testosterone, and a comparison with findings in 159 patients with hirsutism of functional origin reveal the following 1) An androgen-producing tumor must be ruled out when peripheral testosterone exceeds 2 ng/ml; 2) an ovarian venous testosterone level exceeding 20 ng/ml generally accompanies a tumor, particularly when the tumor is less than 5 cm in diameter; and 3) virtually all (98%) of the tumors reviewed were accompanied by virilization, regardless of the peripheral concentration of testosterone.
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PMID:Peripheral and ovarian venous concentrations of various steroid hormones in virilizing ovarian tumors. 21 47

Multiple lutein cyst (MLC) and luteoma are two aspects of ovarian hyperplasia induced by high levels of human chorionic gonadotrophin (HCG). Using a case report of MLC, the authors compare it with luteoma (the anatomoclinical and pathogenic data). Luteoma are more frequent with multipara, whereas MLC are more often seen with paucipara. Maternal virilization can occur in both cases but MLC does not seem to be responsible for fetal virilization. The fetus could be protected by the placenta, thanks to increased aromatase activity and sex binding globulin production. MLC and luteoma are usually found by chance. The pathology must be known, because of their spontaneous regression after delivery. So, the attitude will be conservative under the control of biopsies.
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PMID:[Luteinized cystic hyperplasia of the ovaries during pregnancy. A case report]. 132 53

It has been suggested that sex differentiation in vertebrates is steroid hormone dependent, that estrogens play a critical role in ovarian differentiation, and that male sex differentiation will occur in the absence of estrogens. Using the model of the alligator in which sex can be manipulated by incubation conditions (eggs incubated at a constant temperature of 30 degrees produce 100% females, and at 33 degrees produce 100% males), a series of experiments using antiestrogens, antiandrogen, estradiol-17 beta, dihydrotestosterone (DHT), and aromatase inhibitors were performed. Test substances were injected into alligator eggs prior to gonadal sex differentiation and the eggs were incubated at male or female temperatures until just before expected date of hatching. Gonads were excised and the sex was verified histologically. Control embryos injected with vehicle produced the expected sex: females at 30 degrees and males at 33 degrees. Estradiol in eggs at 33 degrees (male temperature) produced 100% females and did not alter female development in eggs at 30 degrees. Antiandrogen, DHT, and a steroid antiestrogen had no discernible effect in either the 30 degrees or the 33 degrees eggs at the doses tested. The aromatase inhibitors aminoglutethimide and 4-hydroxyandrostenedione caused a moderate disruption of ovarian development and had no apparent effect on testicular development. The nonsteroidal aromatase inhibitor, Ciba Geigy 16949A, caused inhibition of ovarian development in all treated embryos. The Mullerian ducts did not appear to be affected by this treatment, or by any of the other treatments, and the gonads did not appear masculinized. We conclude that estrogen appears to be necessary for normal ovarian development, but that inhibition of estrogen synthesis alone is insufficient to cause masculinization. Likewise, exogenous androgens appear unable to masculinize embryonic gonads. The evidence suggests that testicular differentiation in amniote vertebrates is dependent on factors other than androgens or level of estrogens.
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PMID:Disruption of ovarian development in alligator embryos treated with an aromatase inhibitor. 138 96

Cerebral androgen aromatization has been described as a mechanism responsible for masculinization of the brain, and monoamines seem to be involved in sexual differentiation of the brain. The aim of this study was to investigate the possible implication of monoamines in the masculinization of the brain induced by cerebral androgen aromatization not only in the classic hypothalamic areas but also in some extrahypothalamic ones. For this purpose, 1-day-old male Wistar rats were injected intraventricularly with 5 mg/kg of a suspension of an aromatase inhibitor, LY43578. Saline was administered to male and female control groups. At adulthood, open-field, heterotypical, and homotypical sexual behavior tests were performed and cerebral amines were determined by HPLC-ED. Behavioral tests revealed feminine-like exploratory activity and defecation rate in the treated group, as well as an 89% lordotic response and decreased number of mounts plus intromissions. Testosterone levels were not affected by the treatment. Striatal and limbic serotonergic metabolism showed a sexual dimorphism, higher in males than females, that disappeared in the treated group. From these results, we suggest a possible role of extrahypothalamic serotonin in the mediation of the estrogen-induced mechanisms of behavioral sexual differentiation.
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PMID:Role of monoamines in the male differentiation of the brain induced by androgen aromatization. 159 41

One of the best examples for sex hormone regulation of brain development is found in songbirds. In zebra finches, only males sing because of striking sex differences in the neural circuitry that controls songs. Because developing females treated with estradiol (E2) develop a masculine song system, E2 is considered the normal masculinizing hormone. However, questions about the role of E2 in male development persist, because E2 treatments that masculinize song can demasculinize other sexual behaviors, and there exists contradictory evidence for high levels of circulating E2 in developing males. We remeasured plasma steriods in zebra finches during the first 13 days after hatching. E2 circulated at low levels, and there were no sex differences in circulating E2, estrone, testosterone, androstenedione, or dihydrotestosterone. We also measured aromatase activity [( 3H]androstenedione conversion to [3H]estrone and [3H]E2) in gonad, adrenal, brain, and other tissues of hatchlings. Aromatase was abundant in ovary, but was not definitively detected in testes, adrenals, or other nonneural tissues of males. Aromatase was also found in diencephalon and in high amounts in telencephalon, but sex differences were not detected in whole brain or cellular subfractions of telencephalon. Because ovarian steroidogenesis is high, it may be involved in differentiation of the female zebra finch, as in nonpasserine birds. By contrast, the functional estrogen necessary for masculinization of song is most likely derived from brain, supplied with substrate from the adrenals. The puzzle remains why the song system is not masculinized in females, who possess high levels of aromatizable androgens and telencephalic aromatase.
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PMID:Plasma sex steroids and tissue aromatization in hatchling zebra finches: implications for the sexual differentiation of singing behavior. 172 4

A description is presented of the first documented case of placental aromatase deficiency. The deficiency caused maternal virilization during pregnancy and pseudohermaphroditism of the female fetus. A 24-yr-old primigravida showed progressive virilization during the third trimester. Urinary excretion of estrogen was less than 14 mumol/day between 35-38 weeks of pregnancy, although nonstress tests showed reactive patterns and serum levels of human placental lactogen were above 460 nmol/L. Maternal serum levels of estrogens were low, and those of androgens were high in the third trimester. A dehydroepiandrosterone sulfate loading test induced a marked increase in maternal serum levels of androgens, whereas no such increase was observed in estrogens. The woman delivered vaginally a live full-term infant who exhibited female pseudohermaphroditism. Cord serum levels of estrogens were extremely low, while those of androgens were high. The aromatase activity of the placenta, determined by the conversion of [7-3H]androstenedione to 17 beta-[7-3H]estradiol and [7-3H]estrone, were less than 0.03 fmol/microgram protein.min (control, 9.6 +/- 2.2 fmol/microgram protein.min). The sulfatase activity of the placenta was 0.63 pmol/microgram protein.min compared to 0.46 +/- 0.16 pmol/microgram protein.min in controls. The rate of aromatization by normal control placentas was the same as that obtained during coincubation of samples of normal placentas and that of the patient. Thus, the presence of aromatase inhibitor in the patient's placenta was excluded.
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PMID:A new cause of female pseudohermaphroditism: placental aromatase deficiency. 182 97

Sexual behavior in laboratory rats is influenced by a variety of factors in the perinatal environment. Male rats are masculinized and defeminized in response to circulating testosterone perinatally. Females undergo a process of feminization but in some cases are exposed to testosterone. Previous work has shown that during prenatal development female rats normally undergo a partial masculinization and defeminization of sexual behavior as reflected by altered responsiveness to gonadal hormones in adulthood. In the present study we investigated whether the maternal ovary influences adult females' responsiveness to gonadal hormones. Pregnant rats were ovariectomized on Day 10 of pregnancy and their offspring tested for sexual behavior in adulthood. Following ovariectomy pregnancies were maintained by administration of systemic progesterone. In addition the ovariectomized pregnant rats were given one of three daily treatments (Days 10-21): 0.2 microgram estradiol benzoate in sesame oil and 0.1 cc propylene glycol, 5 mg of the aromatase inhibitor 1,4,6-androstatriene-3,17-dione (ATD) in 0.1 cc propylene glycol, or 0.1 cc propylene glycol. A control group was generated from SHAM operated mothers given daily control injections of propylene glycol and sesame oil. Offspring were ovariectomized in adulthood and tested for display of feminine sexual behavior in response to estradiol benzoate and progesterone or estradiol benzoate alone. Masculine sexual behavior was measured in response to testosterone propionate (TP). Feminine sexual behavior was enhanced in offspring from ovariectomized mothers given only progesterone replacement during pregnancy. Offspring from mothers treated with ATD displayed the greatest elevations in feminine sexual behavior. Estradiol treatments of ovariectomized mothers prevented the increase in feminine potential seen in offspring in the other groups.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:A prenatal source for defeminization of female rats is the maternal ovary. 355 31

Male pseudohermaphroditism due to partial androgen insensitivity (PAI) may be suspected clinically in case of incomplete masculinization of external genitalia in spite of age related plasma androgen levels. In 25 children or adolescents in whom PAI was suspected, the 5 alpha-reductase activity of external genitalia fibroblasts, the number of androgen receptor sites (Bmax) and the affinity of receptors for dihydrotestosterone (Kd) were studied. Clinical expression of PAI is highly polymorphic (Prader's type I to type IV), when most children (18/25) were considered as males. In a single patient the very low 5 alpha-reductase activity permitted the diagnosis of 5 alpha-reductase deficiency. The number of receptor sites (fmoles/mg DNA) varied from 0 to 730. Mean Bmax of patients (282 +/- 187 fmoles/mg DNA) was statistically lower than that of normal subjects (642 +/- 220 fmoles/mg DNA), p less than 0.05. The 5 cases in whom receptor concentrations were normal may be related to a qualitative abnormality of the androgen receptor or to a "post-receptor" defect. On the contrary no significant differences in Kd values were found. Correlation between sexual ambiguity and the number of measured receptors was not possible. These results emphasize the clinical and biochemical heterogeneity of PAI. Nevertheless, the decrease in number of androgen receptor sites remains the major data for the biochemical diagnosis of PAI. Study of post-receptor "markers" (3 alpha-reductase activity, aromatase, collagen) might allow better analysis of cases with PAI in whom androgen receptor concentrations are normal.
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PMID:[Male pseudohermaphroditism caused by partial insensitivity to androgens. Clinical and biochemical heterogeneity]. 408 89

Our scientific language is often misleading. We speak, for example, of virilizing progestins when we should be speaking of "dihydrotestosterone-like" progestins because genital virilization is normally brought about by DHT. We speak of the anti-libidinal properties of antiandrogens as though we knew that their mechanism of action was through the blockage of androgen receptors; some of these agents are antiestrogenic and progestational as well. Until we know the mechanism of action of androgens, estrogens, antiandrogens, antiestrogens, aromatase inhibitors, and reductase inhibitors we should be cautious in our terminology. All hormones and their antagonists have multiple effects.
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PMID:Multiple actions of steroids and their antagonists. 624 Feb 42

17 cases of peristant pubertal gynecomastia (which differs from physiologic breast enlargement by their volume and duration) were studied. Plasma estrogens and urinary phenol steroids excretion were found higher than in normal boys. The main biological finding in these subjects was a decrease of the plasma testosterone/estradiol ratio, and a moderate but transient increase in plasma prolactin. LH and FSH were within the normal range. In the mammary tissue, no estrogen receptor was detectable and aromatase activity was in the same range as in adipose tissue. Pathological examination showed a simulataneous proliferation of galactophoric and fibroblastic stroma. Thus, persistant pubertal gynecomastia could be related to an elevated sensitivity of the mammary tissue to a moderate increase of plasma estrogens. Such a sensitivity could be due to an insufficient masculinization of the mammary anlage during the intra-uterine life.
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PMID:[Persistant pubertal gynecomastia. Biological study (author's transl)]. 625 3


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