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PubMed1980

Spontaneous testicular neoplasm in mice with testicular feminization.

Testicular neoplasms occur spontaneously in androgen insensitive mice with testicular feminization (tfm/y); they are composed of Leydig cells, lipid-laden cells, fibroblastlike cells, and macrophages. The small Leydig cells in the periphery of the tumor are structurally similar to nontumorous tfm/y Leydig cells, whereas centrally located large Leydig cells contain numerous lipid droplets, mitochondria with tubular cristae, and abundant smooth endoplasmic reticulum. The lipid-laden cells exhibit a crescentic nucleus which is displaced toward the periphery of the cytoplasm by a large lipid vacuole. The fibroblastlike cells have a large amount of rough endoplasmic reticulum, lysosomes, free ribosomes, and lipid vacuoles. Macrophages are characterized by numerous layered and dense osmiophilic structures closely associated with crystalshaped bodies. An in vitro study shows that, in comparison with the normal testes, the tfm/y tumors produce significantly less testosterone but a larger quantity of androstenedione. Also, the tumors are capable of converting progesterone to estrone and estradiol-17 beta. The plasma level of testosterone is significantly lower in tumor-bearing animals than in normal littermates, but slightly higher than in the nontumorous tfm/y animals. Since the abnormal steroid enzyme activity is found in both tumor-bearing and nontumorous tfm/y mice, the basic cause of aberrations in sex steroid production appears to be genetic rather than the direct result of alterations in their Leydig cells.

Androgen-Insensitivity Syndrome↗
PubMed1978

Comparative studies in two cases of testicular feminization syndrome, one with and the other without the fluorescent distal band q12 of the Y.

In two patients with testicular feminization syndrome, one Yq12-positive and the other Yq12-negative, we compared phenotype, gonadal histology and ultrastructure, in vivo steroid response of the testes to the administration of exogenous gonadotropin during adrenal suppression, and of the adrenal gland to ACTH. The assumption that the constitutive Y heterochromatin could function as a regulator of steroid biosynthesis and metabolism, with or without effect at other levels, was not firmly supported by the observations reported here. However, further studies along this line may help elucidate the biologic role of this portion of the Y chromosome in humans.

Adrenal Glands↗
PubMed1978

Effect of the mouse mutants testicular feminization and sex reversal on hormone-mediated induction and repression of enzymes.

The mouse mutants testicular feminization and sex reversal have been used to investigate hormone-mediated induction and repression of enzymes. Tfm/Y animals were already known to be androgen insensitive, rendering the androgen-inducible enzymes ADH and beta-glucuronidase noninducible because of an inherited deficiency of a cytosol androgen-receptor complex. The animals display female secondary sexual characteristics. Sxr/+,XX animals display male primary and secondary sexual characteristics with small testes. We demonstrate (1) that the Tfm mutation is pleiotropic, preventing repression of an androgen-repressible enzyme (ornithine aminotransferase) as well as induction of androgen-inducible enzymes, (2) that an estrogen-inducible enzyme (histidine decarboxylase) is not affected by the Tfm mutation, and (3) that Sxr/+,XX animals produce enough androgen for malelike activities of androgen-sensitive enzymes. It was also discovered that histidine decarboxylase repressed by androgen in normal animals, rather than being unaffected by it in Tfm/Y animals, is in fact induced. This unexpected phenomenon is discussed and an explanation is suggested for it.

Alcohol Oxidoreductases↗
PubMed1986

Autoradiographic studies with 3H dihydrotestosterone in the brain of sex reversed mice, heterozygous for androgen insensitive testicular feminization (Tfm). A comparison with normal female mice and sex reversed male mice.

Specific binding sites for 3H dihydrotestosterone are demonstrated by autoradiography in brain nuclei of sex reversed mice heterozygous for testicular feminization (Tfm) which are phenotypically intersexes with testes and accessory sex glands that consist of a mosaic of androgen insensitive Tfm cells which lack specific dihydrotestosterone binding and androgen sensitive normal cells. The nuclear group evaluated include: nucleus (n.) septi lateralis, n. interstitialis striae terminalis, n. medialis amygdalae, the hypothalamic n. arcuatus, n. ventromedialis lateralis, n. pre-mammillaris ventralis, n. preopticus medialis, and nuclei of the cranial nerves VII, X, and XII. In the sex reversed males and the female, used as controls, the frequency of neurons with specific DHT binding show a distinct male-female difference in the caudal part of the arcuate nucleus. In the sex reversed Tfm heterozygotes, in all brain nuclei studied, the frequency of labeled neurons is reduced. The extent of reduction of androgen binding in the different brain nuclei varies among as well as within individual sex reversed Tfm heterozygotes, suggesting variations of the ratio of normal to Tfm neurons in sex reversed Tfm heterozygotes. The differentially reduced androgen binding of different brain systems corresponds to a differentially reduced androgen dependent behaviour reported in the literature.

Amygdala↗
PubMed1988

TfmLac: a second isolation of testicular feminization in mice.

TfmLac, a new occurrence of the X-linked mutation testicular feminization, has been isolated in a stock of mice and mapped to the same region as the original TfmH mutation. We compared these two mutants to determine if there are differences in their putative residual androgen receptors or androgen responsiveness. Such differences have been reported for Tfm mutations in humans. We found no evidence for induction of ornithine decarboxylase (ODC) activity in TfmLac despite androgen treatment for up to 3 weeks. This is in agreement with findings for TfmH. Both of these mutants expressed small amounts of androgen binding activity which shared some properties with the normal androgen receptors in mouse kidney. The binding was distinguishable between the two mutants, however, as determined by hormone saturation experiments utilizing DNA-cellulose chromatography. These findings confirm the independence of the two mutations and are consistent with their being allelic: both result in severe deficits of androgen binding and response.

Androgen-Insensitivity Syndrome↗
PubMed1976

Ultrastructural study of testis in testicular feminization.

Testicular tissue was investigated by electron microscopy in a case of testicular feminization. The seminiferous tubules were lined by spermatogonia and by Sertoli cells. Spermatocytic maturation was not observed. Leydig cells were numerous and contained well developed, abundant vesicular smooth-surfaced endoplasmic reticulum and large mitochondria with tubulovesicular cristae. Reinke crystalloids were absent. The ultrastructural findings were consistent with the assumption that Leydig cells were under adequate stimulation and were in a stage of active secretion. Hence, the results seem to indicate that testicular endocrine function was maintained in the studied case.

Adult↗
PubMed1976

Two feminized male American Indians.

Two American Indian males are described who wish to change sex. Both appear to be anatomically normal; one is a monozygotic twin. In both cases, feminine identification began very early in life. In both cases, there were early acceptance and positive reinforcement of the feminine behavior. These two males and the environment in which they live are contrasted with the anthropological literature published decades ago describing the unique Indian tribal role played by feminized males.

Adult↗
PubMed1977

Central aromatization of testosterone in testicular feminized mice.

Aromatization of testosterone was examined in hypothalamic and cerebral cortex tissues from 32 mice--10 normal males, 10 normal females, 2 carrying the testicular feminized gene (Tfm) and 10 Tfm with the modifying (Ohv) gene. Total aromatization was 1.5 times greater in normal males than females. In both forms of Tfm, conversions were equal and similar to normal females.

Androgen-Insensitivity Syndrome↗
PubMed1987

Effect of exogenously administered estrogens on luteinizing hormone release in a complete testicular feminization syndrome patient with very low testosterone levels, before and after gonadectomy.

The response of LH to exogenously administered estrogens was evaluated in a 63-year-old patient affected by complete testicular feminization syndrome (CTFS) with very low testosterone (T) levels, before and after gonadectomy. Prior to gonadectomy a durative fall in gonadotropin levels was observed after estrogen administration, without observing of an estrogenic positive feed-back (EPF) from LH. After gonadectomy, following an initial decrement in both gonadotropins, the characteristic. LH peak was seen, 48 h after E2B (Estradiol Benzoate) administration. This observation, together with the very low T levels that we found in this patient, prompted us to construe that absence of EPF in males is not due, as previously believed, to a direct inhibitory action of T or E2, deriving from T aromatization, on the hypothalamus, but by a still unknown gonadal factor. The hypothesis that this factor has a tubular origin is formulated and discussed.

Androgen-Insensitivity Syndrome↗
PubMed2006

Increased egg estradiol concentration feminizes digit ratios of male pheasants (Phasianus colchicus).

The length ratio between individual digits differs between males and females in humans, other mammals, lizards, and one bird species. Sexual dimorphism in digit ratios and variation among individuals of the same sex may depend on differential exposure to androgens and estrogens during embryonic life. Organizational effects of sex hormones could cause the observed correlations between digit ratios and diverse phenotypic traits in humans. However, no study has investigated experimentally the effect of prenatal estrogens on digit ratios. We analyzed the effect of estradiol injection in ring-necked pheasant (Phasianus colchicus) eggs on digit ratios. Males from control eggs had higher ratios between the second or third and the fourth digit of the right foot compared to females. Estradiol-treated eggs produced males with lower (feminized) right foot second to fourth digit ratio. Thus, we provided the first experimental evidence that prenatal exposure to physiologically high estrogen levels affects bird digit ratios.

Animals↗
PubMedDate not supplied

Testicular feminization: radiologic considerations in a unique form of cryptorchidism.

A case report of complete testicular feminization is presented. The medical and radiological characteristics of this condition which distinguish it from male cryptorchidism and other disorders of sexual differentiation are discussed. To our knowledge, only three previous case reports have been published in the radiology literature. Our report is the first to describe MRI findings.

Adult↗
PubMed1979

Hypothalamic-pituitary responses to high concentrations of gonadal steroids in a three-month-old infant with a feminizing gonadal stromal tumor.

A 3-month-old female infant feminized by an ovarian stromal tumor is presented. Clinicopathologic aspects of such tumors occurring in infancy are discussed. In addition, the evaluation of hypothalamic-pituitary function preoperatively and postoperatively are presented. In the preoperative, high-steroid environment, both basal and stimulated secretion of follicle-stimulating hormone (FSH) was suppressed. Secretion of luteinizing hormone (LH) was normal. Following surgical castration, stimulated secretion of both gonadotropins clearly increased. These findings suggest an active but less sensitive negative feedback mechanism for FSH than for LH during infancy, i.e., high concentrations of gonadal steroids are necessary to maximally suppress FSH secretion while normal steroid concentrations appear to maximally suppress LH secretion. Developmental changes in hypothalamic-pituitary sensitivity to negative feedback controls are discussed in light of these findings.

Female↗
PubMed1983

Gonadotropins and gonadal steroids in androgen insensitivity (testicular feminization) syndrome: effects of castration and sex steroid administration.

Gonadotropin control mechanisms were examined in 12 subjects with the complete syndrome of androgen insensitivity (testicular feminization). This study confirmed the presence of elevated luteinizing hormone (LH) and normal follicle-stimulating hormone (FSH) values in these subjects and suggests an intact feedback mechanism for FSH but not LH. This gives further credence to the opinion that estrogens and a nonsteroidal inhibin are important in FSH control. Because of an exaggerated pulsatile pattern of gonadotropins in intact and gonadectomized subjects, there were dramatic variations in gonadotropin levels. After gonadectomy, there was a marked rise in FSH and a further rise in LH. Administered estradiol benzoate and, to a lesser degree, testosterone propionate were capable of lowering LH levels. The effect of testosterone could be via conversion to estrogen(s) in the testes or elsewhere.

Adolescent↗
PubMed1985

Feminization of the hepatic monooxygenases by growth hormone is mimicked by puromycin and correlates with a decrease in male-type cytochrome P450.

The hepatic monooxygenase system (MFO) was studied in hypophysectomized male rats treated with growth hormone (GH), puromycin, or both. GH significantly decreased the amount of cytochrome P450 and the activity of ethylmorphine demethylase but did not affect aniline hydroxylase or NADPH cytochrome c reductase. Puromycin significantly increased the activity of the reductase but otherwise had effects identical to GH. The agent's effects were additive. By labelling the P450 with [3H]-heme we found that GH decreased the amount of male-type (slow turnover) P450 by 56% but lowered the female-type (fast turnover) by only 10%. The hormone increased the half-life of both types by 56 and 100% respectively. We conclude that GH feminizes the MFO by decreasing the synthesis of male-type cytochrome P450.

Aniline Hydroxylase↗
PubMed1985

[Mechanism of the refractory state of androgen hormone in Armadillidium vulgare Latr. (crustacean, isopod, oniscoid) harboring a feminizing bacteria].

In thelygenous lines of Armadillidium vulgare, neo-females and intersex males (iM) with feminizing symbiotic bacteria are not masculinized by an extract from iM androgenic gland, which, however, masculinizes bacterialess genetic females. Injection of iM hemolymph extract masculinizes these genetic females. This indicates that androgenic hormone is present in iM hemolymph. Lack of androgenic hormone activity in thelygenous lines is supposed to result from the action of bacteria on the androgenic hormone receptors. Since a temporary recovery of the male differentiation of iM can be induced by implantation of different parts of central nervous system, bacteria effect is probably indirect, through an action on a neurosecretory system, perhaps one of those controlling the functioning of the androgenic gland.

Androgens↗
PubMed1983

Residual androgen binding in testicular feminization (TFM).

Most mutants with genetic androgen-resistance possess some level of androgen binding which exhibits properties of receptors. The present studies aim to determine whether the androgen binding activities in mutants are, or are related to, receptors. This binding portion is termed residual androgen receptors. We have examined several androgen-resistance mutants with testicular feminization (TFM). Putative androgen receptors from mice, rats, and humans with TFM have been compared, and at least three different types of residual receptors have been observed. They are discussed in relation to possible receptor defects and to differences in the nature of androgen-resistance associated with each of them.

Androgen-Insensitivity Syndrome↗
PubMed1983

Zinc metabolism in testicular feminization and surgical cryptorchid testes in rats.

Rats with testicular feminization (Tfm) had been reported to have a testis specific zinc deficiency. In this report it is demonstrated that this organ specific zinc deficiency was not corrected by intraperitoneal zinc administration. Normal littermates on the other hand showed a positive testicular response to zinc administration. The increased testicular zinc level in control animals returned to normal 1 week after the zinc treatment probably due to the fast turnover of this element in the testis. Not only surgically induced cryptorchidism but also surgical cryptorchidism and epididymodeferentectomy (to simulate Tfm conditions in normal adult rats) caused a drastic reduction in testicular zinc level. Unlike in Tfm rats, however, the decrease in zinc content in operated animals was not accompanied by a corresponding decrease in alkaline phosphatase activity. Zinc concentration and alkaline phosphatase activity in plasma or other organs were not affected by the surgical procedure. The testicular copper content in the operated animals was higher than that of the unoperated controls.

Alkaline Phosphatase↗
PubMed1987

Absence of a 23 kd protein in testes of testicular feminization rat.

Cryptorchid testes of testicular feminization rats are very low in zinc in spite of normal zinc status of the animals. Analysis of the cytosol of the cryptorchid testes by gel permeation chromatography showed decreased zinc binding by proteins eluted at fractions corresponding to 30,000 dalton. Further analysis by sodium dodecylsulphate polyacrylamide gel electrophoresis indicated the absence of a protein with molecular weight of 23,000.

Androgen-Insensitivity Syndrome↗