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PubMed1984

Further studies of auxin and ACC induced feminization in the cucumber plant using ethylene inhibitors.

The present study was designed to establish the role of an essential hormone controlling sex expression in cucumber. A potent anti-ethylene agent, AgNO3, completely inhibited pistillate flower formation caused by IAA, ACC or ethephon. Inhibitors of ethylene biosynthesis, AVG and CoCl2 also suppressed feminization due to exogenous IAA or ACC. Though AVG also suppressed ethephon-induced feminization, this may be due to the second effect of AVG rather than the effect on ACC biosynthesis. These results confirm that ethylene is a major factor regulating feminization and that exogenous auxin induces pistillate flower formation through its stimulation of ethylene production, rather than ACC production.

Amino Acids↗
PubMed1998

[Virilizing and feminizing adrenal syndrome].

OBJECTIVE: To inquire into diagnosis, differential diagnosis and treatment of virilizing and feminizing adrenal syndrome especially differential diagnosis between benign and malignant of sex hormone producing adrenal neoplasma and treatment principles of congenital adrenal hyperplasia (CAH). METHOD: Eight cases of CAH and five cases of sex hormone producing adrenal neoplasma were presented during 1986-1996. The former included 3 rare cases of 17 alpha hydroxylase deficiency and others. The latter included 3 cases of feminizing adrenal tumors and 2 cases of virilizing adrenal tumors. RESULT: Weight and diameter of tumor, DHEA, 17-ks and sex hormone levels, appearance of CT imaging, infiltration and metastasis, were closely related to differentiation of benign and malignant tumors. CONCLUSION: Some standards are not absolute because of limited practice, follow-up is very important. Adrenal virilizing and feminizing neoplasms were surgically resected by different incision. Modified subcostal incision is recommended as a best choice for huge adrenal mass. Corticoadrenal hormone treatment of CAH should select different kind of corticoadrenal medicine for different kind of CAH. Treatment of sex hormones is not suitable for children suffered from 17 hydroxylase deficiency until prepuberty.

Adrenal Gland Neoplasms↗
PubMedDate not supplied

[Sex correction in testicular feminization syndrome].

From 1993 to 2000 the authors observed 10 patients with testicular feminization. In spite of existent highly informative methods, early diagnosis of the genesis of abnormal sexual differentiation is not easy, it requires time. Treatment policy varied with the form of testicular feminization. In a complete form (6 patients), bilateral ventrofixation of the gonads (ovotestis) was made, in incomplete form (4 patients) male gonads were removed with subsequent replacement hormonotherapy. Correction of the external genitalia consisted in amputation of the hypertrophic clitoris with creation of the female-type external genitalia. It is emphasized that in incomplete testicular feminization surgical correction should be started before the appearance of secondary sexual characters to raise effectiveness of hormone treatment in formation of a female genotype.

Adolescent↗
PubMed1992

Testicular feminization syndrome in a mare.

Testicular feminization syndrome was diagnosed in a mare with aggressive, stallion like behavior and a history of infertility. She was found to have a high baseline testosterone concentration suggesting that testicular tissue was present, and ovarian-like structures examined by use of transrectal ultrasonography had the appearance typical of testicular tissue. Although her external female genitalia appeared normal, her vagina ended in a blind sac, and no cervix or uterus were identified. Surgery was performed, and structures removed from the abdominal cavity were determined to be hypoplastic testicles. Removal of the testicular tissue resulted in complete resolution of her aggressive behavior. Chromosomal evaluation revealed that the mare had 64X,Y (normal male) karyotype. Testicular feminization syndrome is a condition characterized by insensitivity of reproductive tissues to androgens during development because of an abnormality in androgen receptors. This androgen insensitivity results in development of normal external female genitalia, with high testosterone concentrations being released from developing testicles. Testicular feminization syndrome has not been commonly diagnosed in horses, but should be considered as a differential diagnosis for overly aggressive mares with a history of infertility.

Aggression↗
PubMed1988

Testicular feminization syndrome.

The testicular feminization syndrome occurs as a result of faculty genetic programming. This inherited condition causes an XY male embryo to develop into a person who has an XY karyotype and a female appearance. The described individual appears "female" at birth and is naturally socialized as a female. A testicular feminized "female" may seek routine health care at a primary health care center. Upon examination, certain identifying physical characteristics may be observed. Primary amenorrhea and infertility are inherent characteristics of the condition. This article describes the testicular feminization syndrome, its etiology/pathophysiology and both subjective and objective findings. Nursing interventions such as data collection, family tree charts, Barr body screening, education, referral and counseling are suggested. Nurse practitioners have the opportunity to identify suspected cases and direct those individuals toward appropriate treatment and discreet counseling. Counseling generally will emphasize that the TFS individual may consider herself female.

Androgen-Insensitivity Syndrome↗
PubMed1993

[A case of neurinoma combined with testicular feminization syndrome].

A 23-year-old female was admitted to our hospital because of a mediastinal tumor. She complained of primary amenorrhea, and abdominal echosonography was therefore performed, revealing the absence of a uterus. Chromosome analysis revealed a 46 XY genotype, indicating the patient to be a male, not a female. Left renal venography demonstrated residual blood vessels originating in the Mullerian ducts. Thoracotomy and laparotomy were performed, and the mediastinal tumor and bilateral testes were resected. Postoperative pathology revealed that the mediastinal tumor was a neurinoma. There was no spermatogenesis, but hyperplasia of Sertoli cells in the testes was seen. Neither the neurinoma nor the testes were malignant. Bioassay of the testes showed no androgen receptors, leading to the diagnosis of testicular feminization syndrome with the complete form of androgen insensitivity. There have been many reports of an association between testicular feminization syndrome and malignant tumors of the testes, but few reports of an association between testicular feminization syndrome and benign tumors such as neurinoma. Accordingly, the present case was considered to be unusual and worth reporting.

Adult↗
PubMed1980

Feminization in hepatocellular carcinoma corrected by chemotherapy: a case report.

A 17-year-old boy with metastatic hepatocellular carcinoma and feminization became asymptomatic after administration of antineoplastic agents. Serum estradiol level, urine estrogens, and tumor estrogen receptors were changed after the treatment. Achievement of partial remission resulted in normalization of the serum sex hormone profile and disappearance of the feminization in spite of the presence of residual tumor. Thus, serum hormone levels alone cannot be used as tumor markers for control of therapy. This suggests that chemotherapy may have altered the biological behavior of the tumor, which resulted in loss of its ability to synthesize estrogen estrogen receptors.

Adolescent↗
PubMed1991

Mechanism of feminization in male patients with non-alcoholic liver cirrhosis: role of sex hormone-binding globulin.

We measured serum sex hormone-binding globulin (SHBG) using a radioimmunoassay developed by us, testosterone (T), estradiol (E2), free T and free E2 in 50 male patients with non-alcoholic liver cirrhosis (compensated: 30, decompensated; 20) and age-matched healthy male subjects, SHBG was significantly increased in patients with liver cirrhosis compared with healthy subjects. The high serum SHBG level in male compensated cirrhotic patients tended to decrease with progression to the decompensated state. Serum cholinesterase showed a positive correlation with SHBG in liver cirrhosis. Serum free T and the T/SHBG ratio decreased, while serum E2, free E2, and the E2/T and the free E2/free T ratios increased in liver cirrhosis, resulting in estrogen predominance and feminization of male patients. These changes were more marked in decompensated than compensated liver cirrhosis. An increased free E2/free T ratio was observed in patients with gynecomastia, palmar erythema or vascular spider. The T/SHBG ratio showed a positive correlation with serum free T, suggesting that it can be used as a free T index in liver cirrhosis. From these observations, it is suggested that serum SHBG plays an important role, by regulating the serum free T level in the occurrence of feminization in male patients with non-alcoholic liver cirrhosis.

Adult↗
PubMed1988

Effects of feminization of male F344 rats on induction of tumors and on nucleic acid alkylation by nitrosobis-(2-oxopropyl)amine.

Groups of male and female F344 rats were treated twice weekly by gavage with 2.5 mg of nitrosobis-(2-oxopropyl)amine (BOP) for 35 weeks. Additional groups given the same treatment were male rats castrated at birth, male rats bearing an implant of a pellet containing estradiol and castrated male rats bearing an estradiol pellet. Most rats died with tumors related to the treatment; intact male rats survived the least well of the five groups. Most rats in all groups had alveolar/bronchiolar neoplasms of the lung. Many of the male rats also had follicular cell neoplasms of the thyroid and transitional cell neoplasms of the urinary bladder and kidney pelvis; there were no liver tumors in intact male rats. Almost all female rats and castrated male rats had liver neoplasms, including hepatocellular, cholangiocellular and hemangiosarcomatous neoplasms, but few neoplasms of the thyroid, kidney or bladder. The male rats feminized with estradiol, intact or castrated, had liver neoplasms, mainly cholangiocellular, and also neoplasms of the thyroid. Two rats of each of the five groups were treated at 20 weeks of age with [14C]BOP. As measured by respiration of 14CO2, metabolism of BOP was faster in the two groups of male rats with the estradiol implant than in the other groups. DNA and RNA of the liver were isolated 6 h after treatment. The extent of methylation of liver DNA as 7-methylguanine and O6-methylguanine was higher in the females and in the feminized males than in the intact male rats, but when normalized to the dose of nitrosamine per unit body weight there was little difference among the five groups.

Alkylation↗
PubMed2006

Urogenital papilla feminization in male Pomatoschistus minutus from two estuaries in northwestern Iberian Peninsula.

Recently, male urogenital papilla feminization (UGPF) in the sand goby Pomatoschistus minutus was reported in several UK estuaries with high levels of estrogenic compounds. The fact that this species is also common in southern European estuaries, together with its life-cycle characteristics, prompted us to investigate P. minutus UGPF in the northwestern of Iberian Peninsula. Specimens of P. minutus were periodically sampled during 2004 at several locations in two estuaries (Minho and Lima). Evidence for UGPF was recorded in both estuaries, the highest incidence being observed in the Lima estuary (50%). Estrogen levels (17beta-estradiol and estrone) above 100 pg/l were observed in both estuaries, the higher concentrations being found in the Lima estuary. Overall, the results suggest a relationship between the feminization of male P. minutus urogenital papilla and the presence of estrogenic compounds. In the future, more in-depth studies are required in order to use P. minutus as a sentinel species for estrogenic compound monitoring in estuaries.

Animals↗
PubMed2006

Feminizing adreno-cortical carcinomas in male adults. A dire prognosis. Three cases in a series of 801 adrenalectomies and review of the literature.

UNLABELLED: We describe the clinical presentation, biochemical features, diagnostic criteria, clinical course and differential diagnosis in three cases of feminizing adreno-cortical carcinoma (FACC) with a review of the literature. PATIENTS: From 1970 throughout December 2003 among a series of 801 adrenalectomies, three had been performed for FACC. RESULTS: Age at presentation was 74, 63 and 23 years. Estradiol hypersecretion was observed in 3/3 patients, 17 OH progesterone was elevated in 2/3 patients and both of them had a diminution of testosterone, delta 4 androstenedione was elevated in 1/3 patients. Imaging studies suggested malignancy in 3/3 patients by the presence of necrosis, heterogeneity, calcifications, size of the tumor and compression of adjacent organs. All patients were stage III at presentation and had a Weiss score >or=6. Size and weight of the tumors were 30, 20, 15cm and 3750, 480 and 275g respectively. All 3 patients received mitotane and cortisone post-operatively and at follow up (7, 3 and 2 years) all 3 died of the disease. CONCLUSIONS: Feminizing adreno-cortical carcinomas in adults are exceedingly rare (1-2% of adreno-cortical carcinomas). Tumors are huge and even after surgery for cure their prognosis is worse than for other varieties of adreno-cortical carcinomas either secreting or non secreting. Early diagnosis and treatment may improve overall prognosis.

Adrenal Cortex Neoplasms↗
PubMed2004

Remote sensing of intraperitoneal parasitism by the host's brain: regional changes of c-fos gene expression in the brain of feminized cysticercotic male mice.

Experimental intraperitoneal Taenia crassiceps cysticercosis in mice exhibits distinct genetical, immunological and endocrinological features possibly resulting from the complex interactive network of their physiological systems. Very notable is the tendency of parasites to grow faster in hosts of the female sex. It is also remarkable in the feminization process that the infection induces in chronically infected male mice, characterized by their estrogenization, deandrogenization and loss of sexual and aggressive patterns of behaviour. The proto-oncogene c-fos is a sex steroid-regulated transcription factor gene, expressed basally and upon stimulation by many organisms. In the CNS of rodents, c-fos is found expressed in association to sexual stimulation and to various immunological and stressful events. Hence, we suspected that changes in c-fos expression in the brain could be involved in the feminization of the infected male mice. Indeed, it was found that c-fos expression increased at different times during infection in the hypothalamus, hippocampus, less so in the preoptic area and cortex, and not in several other organs. The significant and distinctive regional changes of c-fos in the CNS of infected mice indicate that the brain of the host senses intraperitoneal cysticercosis and may also announce its active participation in the regulation of the host-parasite relationship. Possibly, the host's CNS activity is involved in the network that regulates the estrogenization and deandrogenization observed in the chronically infected male mice, as well as in the behavioural and immunological peculiarities observed in this parasitic infection.

Animals↗
PubMed1983

Prevention of demasculinization and feminization of the brain in prenatally stressed male rats by perinatal androgen treatment.

Female rats were exposed to immobilization and illumination stress from day 15-22 of pregnancy. Their male offspring showed demasculinization, i.e. significantly decreased male sexual behaviour, and feminization, i.e. significantly increased female sexual behaviour, in adulthood. This permanent demasculinization and feminization of the brain, induced by prenatal stress, could be prevented by perinatal androgen treatment.

Androgens↗
PubMed1977

Mechanism of feminization in primary liver cancer.

Primary liver cancer occasionally presents with feminization. The mechanism is unknown. We studied a young man with primary liver cancer associated with feminization that disappeared after removal of the tumor. Before operation, the serum estrone level was markedly (1113 pg per milliliter) and estradiol and estriol levels were slightly elevated. Human placental lactogen was also increased (0.52 microng per milliliter). Luteinizing hormone, follicle-stimulating hormone and prolactin levels were normal, and testosterone reduced. Beta subunits of human chorionic gonadotropin were not detected in the serum. In vitro assay of tumor tissue showed estrogenic activity and high levels of these subunits. With a reversed isotope dilution technic with crystallization to constant specific activity, we showed the tumor tissue to convert dehydroepiandrosterone sulfate and dehydroepiandrosterone to estrone and estradiol. Production of beta subunits of chorionic gonadotropin and raised serum levels of placental lactogen provided further evidence that the tumor was functioning as trophoblastic tissue.

Adult↗
PubMed1981

Bilateral incipient germ cell tumours of the testis in the incomplete testicular feminization syndrome.

The presence of bilateral incipient germ cell tumours in the testes of two cases of the incomplete testicular feminization syndrome (TFS) is reported and found to resemble that occurring in the testes of infertile men. Both the nature and nomenclature of the lesion is discussed, as is its relevance in the early diagnosis and improved therapy of testicular tumours, which occur frequently in TFS. Suggestions are made for a more complete postpubertal surveillance in these patients, including assay of tumour markers and bilateral biopsies in cases of complete TFS. In this condition the removal of the testes is usually delayed until the twenties when total feminization is achieved, thus increasing the chances of tumour development.

Adolescent↗
PubMed1982

Estrogenic feminization of the LH response to orchidectomy in the rat: evidence for a hypothalamic site of action.

These studies were conducted to determine the possible site of action at which estrogen "feminizes" the pituitary luteinizing hormone (LH) response to orchidectomy (ORDX). When Silastic implants containing estradiol-17 beta (E2) were inserted 1 day prior to ORDX and subsequently removed 5 days later, characteristic increases in plasma LH and follicle-stimulating hormone (FSH) levels normally observed within 24 h after ORDX were completely (for LH) or partially (for FSH) prevented. Rather, gonadotropin patterns, especially LH, resembled patterns seen during a similar time interval after ovariectomy of female rats in diestrus-1, that is, increases in plasma FSH unaccompanied by rises in plasma LH. Although castration-induced increments in plasma gonadotropin levels were abated by prior E2 treatment of orchidectomized male rats, the responsiveness of the anterior pituitary gland to two intravenous pulse injections of luteinizing hormone-releasing hormone (LHRH) tested 6 and 8 h after removal of E2 capsules was markedly greater than pituitary LH responses to both pulse injections at similar times following ORDX. Pituitary FSH responses in E2-treated orchidectomized rats were higher only after the second LHRH injection. To determine whether the increased pituitary responsiveness to LHRH was actually due to the E2 treatment or to the concomitant orchidectomy, pituitary LH and FSH responses to a single LHRH pulse injection were evaluated 10 h after removal of either E2 or empty capsules from 4-day orchidectomized rats in which these capsules had been inserted 1 day prior or ORDX. It was found that pituitary LH responses to LHRH were greatly increased 4 days after ORDX. Moreover, mean maximal increments in LH and FSH were significantly higher in ORDX-E2-treated castrated rats. Therefore, the data indicate that E2 delays the onset of increases in plasma LH and to a lesser extent FSH concentrations after ORDX ("feminization") by acting within the hypothalamus to inhibit the release of LHRH from peptidergic neurons.

Animals↗
PubMed1992

Familial adrenal feminization probably due to increased steroid aromatization.

5/10 members of a North African family (father, 2 male and 2 female siblings) had gynaecomastia, early growth and short final stature. The 8-year-old propositus had advanced bone age, facial acne, gynaecomastia, pubic hair and prepubertal testicular volume. Basal oestrone (E1) was elevated (670 pmol/l) and increased with adrenocorticotropic hormone (ACTH; 826 pmol/l). After human chorionic gonadotropin stimulation testosterone (T) responded normally whereas E1 and oestradiol (E2) remained unchanged. ACTH-dependent adrenal feminization was confirmed by a transient reduction of breast tissue following dexamethasone or cypropterone acetate treatment. Testolactone increased T/E2 (from 5.6 to 20.3) and A/E1 (from 3.4 to 31.4) ratios and temporarily reduced the breast tissue. In conclusion, this is a familial type of adrenal feminization with increased adrenal androgen aromatization. This is the first time that male-to-male and male-to-female transmission has been reported.

Adrenal Glands↗