Earnings and feminization of the veterinary profession.
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[Medical demography in Lebanon. Plethora, feminization, youthfulness].
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Adult↗
[Familial occurrence of testicular feminization].
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Adolescent↗
Earnings and feminization of the veterinary profession.
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Earnings and feminization of the veterinary profession.
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Sex determination in polyploids of Caenorhabditis elegans.
In Caenorhabditis elegans triploid animals with two X chromosomes (symbolized 3A;2X) are males. However, these triploid males can be feminized by making them mutant for recessive dosage compensation mutations, by adding X chromosome duplications or by microinjecting particular DNA sequences termed feminizing elements. None of these treatments affects diploid males. This study explores several aspects of these treatments in polyploids. The dosage compensation mutants exhibit a strong maternal effect, such that reduction of any of the dosage compensation gene functions in the mother leads to sex reversal of 3A;2X animals. Likewise, all X chromosome duplications tested cause both sex reversal and intersexual development of many 3A;2X animals. Microinjected feminizing element DNA does not cause extensive sex reversal, but does result in intersexual development in 3A;2X animals. Neither X chromosome duplications nor microinjected feminizing elements show that extreme maternal effect of the dosage compensation mutants, although there is indirect evidence for a maternal effect of the feminizing elements. In particular, very little feminizing element DNA needs to be microinjected in order to feminize triploid males, far less than what is needed for stable inheritance, implying that feminizing elements can work within the mother's gonad. However, even very high concentrations of microinjected feminizing elements do not affect sex determination in diploid males, suggesting that they are not part of the numerator of the X/A ratio. In addition, no pair of X chromosome duplications feminizes diploid males, suggesting that none of these duplications contains a numerator of the X/A ratio. Instead, I infer that an X-linked locus, as yet undefined, must be present in two copies for hermaphrodite development to ensue or that the two X chromosomes might interact.
Animals↗
Ovarian hormones can organize the rat corpus callosum in adulthood.
The rat corpus callosum (CC) is larger in males than females, and is responsive to hormone manipulations during development. Previous data suggest that CC sensitivity to testosterone ends by postnatal day 8 (P8). In contrast, responsivity to ovarian hormones extends as late as P25. The current series of experiments investigates whether ovarian hormone effects on the callosum are permanent and whether CC sensitivity to ovarian hormones extends beyond P25. We found that P70 ovariectomy (Ovx) did not affect callosal size, suggesting that ovarian hormone exposure sometime prior to P70 is sufficient to feminize the CC, and that once the callosum is feminized, the effects can not be reversed. We also found that P25 ovariectomy enlarged, or defeminized, adult female CC, whereas ovary transfer starting on P55 or P70 counteracted this enlarging effect, resulting in feminized adult CC. Thus, although a previously feminized callosum is not affected by P70 ovarian hormone removal, a not-yet feminized callosum can still be feminized after P70. These findings indicate that there is flexibility in the developmental window within which the female brain is responsive to the active feminization process initiated by ovarian hormones.
Age Factors↗
Growth hormone: a regulator of the sexually differentiated steroid metabolism in rat liver.
Specific lesions in the periventricular area of the hypothalamus in male rats lead to a partial feminization of the liver steroid metabolism and a simultaneous reduction of the somatostatin level in the median eminence. Administration of an antiserum against somatostatin causes a similar degree of feminization of liver metabolism in male rats. Thus somatostatin could be the neuroendocrine regulator of the sexually differentiated metabolism of steroids in rat liver. A possible influence from the amygdaloid complex in regulating hepatic steroid metabolism is also indicated since large lesions in the amygdala cause a slight feminization of hepatic steroid metabolism in male rats. The female pattern of hepatic steroid metabolism is induced following frequent administration of hGH. The feminizing effect of hGH on hepatic steroid metabolism does not require the presence of gonads, adrenals, or thyroid. The somatogenic property of hGH seems to be responsible for the feminizing effect since purified rGH alone gives a complete feminization of hepatic steroid metabolism in hypophysectomized animals. rGH purified from male or female pituitary glands is equally efficient in feminizing hepatic steroid metabolism. Furthermore, male or female rGH have the same apparent molecular weight and isoelectric point. The mechanism whereby GH regulates hepatic steroid metabolism could be related to the sexually differentiated secretory profile of GH in the rat. A continuous presence of GH in the circulation seems to be a prerequisite for a female pattern of hepatic steroid metabolism. By analogy, it may be suggested that the high-peak, low-trough secretory pattern of GH characteristic of male rats causes a masculine type of liver steroid metabolism. Gonadal hormones affect both the secretory profile of GH and hepatic steroid metabolism. It is most probable that gonadal hormones affect liver steroid metabolism via modulations of the GH secretory profile. Possibly, estrogen exerts its effect directly on the pituitary by stimulating GH secretion. Androgen most probably has its primary site of action in the anterior hypothalamus or in extrahypothalamic areas. A plausible mechanism is that androgens stimulate the hypothalamic GH-inhibitory center. An overall view of the present hypothesis concerning hypothalamopituitary regulation of the sexually differentiated hepatic steroid metabolism in the rat is presented in Figure 2.
Androgens↗
Regulation of sexually dimorphic hepatic steroid metabolism by the somatostatin-growth hormone axis.
Lesions in the periventricular hypothalamic area in male rats results in a "feminization" of steroid metabolizing enzymes in the liver. These lesions also resulted in a decrease of somatostatin levels in the median eminence. Since blockade of somatostatin by in vivo administration of an antiserum also caused "feminization" of the liver, it is possible that at least one hypothalmic factor responsible for "feminization" is related to somatostatin. Also extrahypothalmic areas seem to influence sexually differentiated functions in the liver. The neuroendocrine control of the "feminizing factor" secretion from the pituitary bears several resemblances to the central control of GH. The hypothesis that the plasma pattern of GH regulates hepatic steroid metabolism in the rat was studied in two different animal models: (1) Different plasma patterns of GH were achieved by administration of human GH (hGH) at different frequencies or by infusing the hormone continuously by means of Alzet osmotic minipumps to hypophysectomized female rats. (2) The plasma pattern of GH in animals with an intact pituitary gland was investigated under conditions which lead to "feminization" of hepatic steroid metabolism. The results demonstrate that the plasma pattern of GH influences hepatic steroid metabolism. Increased trough plasma GH values or absence of time periods with undetectable plasma levels of GH appears to be a major determinant for "feminization" of hepatic steroid metabolism. Since sex steroids were found to influence the plasma pattern of GH it seems as if differences in the plasma pattern of GH between male and female rats explain the sex-differentiated hepatic steroid metabolism.
3-Oxo-5-alpha-Steroid 4-Dehydrogenase↗
Multiple infection with Wolbachia inducing different reproductive manipulations in the butterfly Eurema hecabe.
Wolbachia are rickettsial intracellular symbionts of arthropods and nematodes. In arthropods, they act as selfish genetic elements and manipulate host reproduction, including sex-ratio distortion and cytoplasmic incompatibility (CI). Previous studies showed that infection of feminizing Wolbachia and CI Wolbachia sympatrically occurred in the butterfly Eurema hecabe. We demonstrate that feminization-infecting individuals can rescue sperm modified by CI-infecting males. Phylogenetic analysis revealed that feminized individuals are infected with two distinct Wolbachia strains: one is shared with CI-inducing matrilines, and the other is only found in feminized matrilines. Therefore, the simultaneous double manipulation, CI rescue and feminization, is caused by different Wolbachia strains in feminized individuals, not by a single Wolbachia with two functions. This is the first finding of double infection of Wolbachia with different reproductive manipulations.
Animals↗
Role of the hypothalamo-pituitary-liver axis in sex differences in susceptibility of the liver to toxic agents.
At birth testicular androgens irreversibly program brain centers involved in hypothalamopituitary control of hepatic sex-dependent steroid and drug metabolism. This imprinting process results in activation of a hypothalamic "feminostatin"-a secreting center that is turned on just before puberty. Feminostatin inhibits pituitary secretion of "feminizing factor," a pituitary hormone that feminizes the basal type of metabolism characterizing the liver of hypophysectomized and gonadectomized rats. Consequently, female rats that are devoid of feminostatin will secrete feminizing factor from the pituitary, leading to a feminine type of hepatic metabolism. Male rats have an active feminostatin-secreting center, and inhibition of pituitary feminizing factor release results in an autonomous type of liver metabolism. Female rats show a relative androgen unresponsiveness and seem incapable of releasing feminostatin after treatment with natural androgens, possibly because of more efficient metabolism (breakdown) of androgen in the female than in the male rat brain. 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. No effects were seen in analogous lesions in female rats in any of the cases studied. These 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 feminostatin have their origins in this area of the hypothalamus or may send axons through this area to the basal hypothalamus and thus directly or indirectly influence the anterior pituitary gland. Regulation by the central nervous system of a "lactogenic" (prolactin, Prl) receptor, present in the female rat liver, was also studied. This receptor is present in very low concentration or absent in the male rat. Anterior hypothalamic deafferentation at the retrochiasmatic level in male rats increased the hepatic Prl receptor concentration to the female level 3-4 days following the operation. A transection rostral to the suprachiasmatic nucleus had no effect on the concentration of Prl receptors in male animals. Our results demonstrate that the number of Prl receptors is regulated by the hypothalamo-pituitary system. The receptor-inducing pituitary factor might be related to the feminizing factor. Experiments were carried out to elucidate the nature of the Prl receptor-inducing pituitary factor. Human growth hormone (hGH) continuously administered was shown to induce Prl receptors in livers from male and female hypophysectomized-gonadectomized rats. The prolactin receptors were increased to a level found in control female rat livers. This inductive effect of hGH was also seen in adrenalectomized and thyroidectomized male rats. The induced Prl receptors in male rats had similar characteristics as hepatic Prl receptors in female rats. Also the endogenous rat hormones, rPrl and rGH, were administered in minipumps. In the concentration used (10 mug/mul), rPrl had no effect whereas rGH increased Prl receptor levels to approximately 37% of the female control level. These results indicate that GH or a peptide related to GH may be involved in the regulation of hepatic Prl receptors. The hypothalamo-pituitary-liver axis represents a new concept in endocrine regulation of drug toxicity. The male rat liver has been shown to be more susceptible than the female rat liver to the hepatocarcinogenic action of certain drugs, and it is conceivable that sex differences in the metabolic activation of the drugs in the liver may explain the greater sensitivity of male rats to chemically induced hepatocellular carcinoma. Similar sex differences in liver cancer incidence have been reported in the human.
Aging↗
Gonadal function in chronic alcoholic men.
Alcoholism affects nine million individuals in the United States according to United States Government estimates. As many as 80% of hard-core alcoholic men show evidences of feminization including impotence, testicular atrophy, sterility, gynecomastia and changes in bodily hair. The causes of feminization of male alcoholics have remained obscure until recently. Largely as a result of advances in the techniques of measurement of sex hormones, it has become possible to begin to examine the pathogenesis of feminization. The results of initial studies suggest that alcoholics become feminized through the secondary effects of alcohol-induced liver disease, and also through primary effects of alcohol on the endocrine system. It can be shown that liver disease permits the peripheral escape of steroid precursors and their conversion to estrogenic substances. These substances are then inadequately cleared by the liver. In addition, however, alcohol alters testicular steroidogenesis and testosteronogenesis. Hypothalamic-pituitary function also is diminished in chronic alcoholics, and this change contributes to the syndrome of feminization.
Alcoholism↗
Exposure of juvenile roach (Rutilus rutilus) to treated sewage effluent induces dose-dependent and persistent disruption in gonadal duct development.
Wild roach (Rutilus rutilus) have been found with intersex gonads in rivers throughout the United Kingdom. The incidence of intersexuality is strongly correlated with discharges of estrogenic treated sewage effluent into those rivers, and this has led to the hypothesis that estrogenic chemicals in effluents are feminizing wild male fish. In this study, early-life stage roach (50 days post hatch, dph) were exposed for 150 days to a graded concentration (0%, 12.5%, 25%, 50%, and 100%) of treated sewage (primarily domestic) effluent to examine the effects of exposure on sexual differentiation and development. Measurement of steroid estrogens and alkylphenolic chemicals in the effluent and a resulting dose-dependent induction of vitellogenin (VTG; a female-specific, estrogen-dependent plasma protein) confirmed that the fish had been exposed and responded to "estrogen" in the effluent. Exposure to treated sewage effluent induced feminization of the reproductive ducts in "male" roach in a dose-dependent manner (in full-strength effluent, 100% of the fish had feminized ducts), indicating that the disruption of the gonad ducts seen in wild roach is the result of exposure to treated sewage effluents during early-life stages. There were no effects of treated sewage effluent exposure on germ cell development; therefore, no oocytes occurred in the testes of the feminized male roach. Subsequent, depuration of the effluent exposed fish in "clean" water for 150 days resulted in a reduction in plasma VTG but no alteration of the feminized ducts, indicating that the effect of the treated sewage effluent on reproductive duct development was permanent. The causality of oocytes in the testes of wild male roach therefore remains to be elucidated.
Animals↗
Wolbachia infection in the terrestrial isopod oniscus asellus: sex ratio distortion and effect on fecundity
Maternally inherited Wolbachia bacteria are widespread in arthropods where they are responsible for various reproductive alterations. In terrestrial isopods (woodlice), Wolbachia may induce feminization or cytoplasmic incompatibility (CI), but their effect remains unknown in most host species. To increase our understanding of host/symbiont interactions in terrestrial isopods, the effect of Wolbachia was investigated in the oniscidean Oniscus asellus, mainly to discriminate between feminization and CI. The Wolbachia infection was not linked with a CI phenomenon, but females infected with Wolbachia produced female-biased broods compared with uninfected females. The fecundity of infected females was slightly lower than that of uninfected, but the number of young at the adult stage was similar between the two female categories. The experimental transfer of the symbiont into uninfected strains showed that Wolbachia was responsible for the feminization of a number of genetic males. In female-biased broods, Wolbachia were vertically transmitted to around 88% of the offspring, but the transmission rate was lower in the few male-biased progenies. The feminizing activity of these symbionts was not systematic, as many phenotypic males were infected. These results contrasted with what is known in another woodlouse species, and indicated that feminization has evolved in different ways in terrestrial isopods.
Journal Article↗
Sex determination in the nematode C. elegans: analysis of tra-3 suppressors and characterization of fem genes.
Mutations of the gene tra-3 result in partial masculinization of XX animals of C. elegans, which are normally hermaphrodites (males are XO). A total of 43 tra-3 revertants (one intragenic, 42 extragenic) have been isolated and analyzed, in the hope of identifying new sex-determination loci. Most (38) of the extra-genic suppressors cause partial or complete feminization of XX and XO animals; the remaining four are weak suppressors. The feminizing suppressors are mostly alleles of known sex-determining genes: tra-1 (11 dominant alleles), tra-2 (one dominant allele), fem-1 (four alleles) and fem-2 (four alleles), but 18 are alleles of a new gene, fem-3. Additional alleles have been isolated for the fem-2 and fem-3 genes, as well as fem-3 deficiencies. Mutations in fem-3 resemble alleles of fem-1 (previously characterized): putative null alleles result in complete feminization of XX and XO animals, transforming them into fertile females. Severe alleles of fem-2 also cause complete feminization of XX animals at all temperatures, but feminization of fem-2 XO animals is temperature-sensitive: complete at 25 degrees, incomplete at 20 degrees. As with fem-1, severe mutations of fem-2 and fem-3 are wholly epistatic to masculinizing alleles of tra-2 and tra-3, and epistatic to tra-1 masculinizing alleles in the germline, but not in the soma. All three fem genes are essential for male development and appear to have a dual role in promoting spermatogenesis and repressing tra-1 activity. All three fem genes exhibit strong maternal effects; the maternal contribution of fem gene products may be inactivated in XX animals by a posttranscriptional mechanism. Maternal contributions of wild-type fem-3 product are necessary for normal XO male development and XX hermaphrodite (as opposed to female) development.
Alleles↗
Sex determination in the Drosophila germline is dictated by the sexual identity of the surrounding soma.
It has been suggested that sexual identity in the germline depends upon the combination of a nonautonomous somatic signaling pathway and an autonomous X chromosome counting system. In the studies reported here, we have examined the role of the sexual differentiation genes transformer (tra) and doublesex (dsx) in regulating the activity of the somatic signaling pathway. We asked whether ectopic somatic expression of the female products of the tra and dsx genes could feminize the germline of XY animals. We find that Tra(F) is sufficient to feminize XY germ cells, shutting off the expression of male-specific markers and activating the expression of female-specific markers. Feminization of the germline depends upon the constitutively expressed transformer-2 (tra-2) gene, but does not seem to require a functional dsx gene. However, feminization of XY germ cells by Tra(F) can be blocked by the male form of the Dsx protein (Dsx(M)). Expression of the female form of dsx, Dsx(F), in XY animals also induced germline expression of female markers. Taken together with a previous analysis of the effects of mutations in tra, tra-2, and dsx on the feminization of XX germ cells in XX animals, our findings indicate that the somatic signaling pathway is redundant at the level tra and dsx. Finally, our studies call into question the idea that a cell-autonomous X chromosome counting system plays a central role in germline sex determination.
Alleles↗
Wild intersex roach (Rutilus rutilus) have reduced fertility.
Endocrine-disrupting chemicals, known to be present in the environment, have great potential for interfering with reproductive health in wildlife and humans. There is, however, little direct evidence that endocrine disruption has adversely affected fertility in any organism. In freshwater and estuarine fish species, for example, although a widespread incidence of intersex has been reported, it is not yet known if intersexuality influences reproductive success. The purpose of this study was, therefore, to determine gamete quality in wild intersex roach (Rutilus rutilus) by assessing sperm characteristics, fertilization success, and ability to produce viable offspring. The results clearly demonstrate that gamete production is reduced in intersex roach. A significantly lower proportion of moderately or severely feminized fish (17.4% and 33.3%, respectively) were able to release milt compared with normal male fish from contaminated rivers (in which 97.6% of the males were able to release milt), reference male fish (97.7%), or less severely feminized intersex fish (experiment 1: 85.8%, experiment 2: 97%). Intersex fish that did produce milt produced up to 50% less (in terms of volume per gram of testis weight) than did histologically normal male fish. Moreover, sperm motility (percentage of motile sperm and curvilinear velocity) and the ability of sperm to successfully fertilize eggs and produce viable offspring were all reduced in intersex fish compared with normal male fish. Male gamete quality (assessed using sperm motility, sperm density, and fertilization success) was negatively correlated with the degree of feminization in intersex fish (r = -0.603; P < 0.001) and was markedly reduced in severely feminized intersex fish by as much as 50% in terms of motility and 75% in terms of fertilization success when compared with either less severely feminized intersex fish or unaffected male fish. This is the first evidence documenting a relationship between the morphological effects (e.g., intersex) of endocrine disruption and the reproductive capabilities of any wild vertebrate. The results suggest that mixtures of endocrine-disrupting substances discharged into the aquatic environment could pose a threat to male reproductive health.
Animals↗
Microinjected DNA from the X chromosome affects sex determination in Caenorhabditis elegans.
The signal for sex determination in the nematode Caenorhabditis elegans is the ratio of the number of X chromosomes to the number of sets of autosomes (X/A ratio). By previous genetic tests, elements that feminized chromosomal males appeared to be widespread on the X chromosome, but the nature of these elements was not determined. In experiments to define a feminizing element molecularly, cloned sequences were added to chromosomally male embryos by microinjection into the mother. Three different X-chromosome clones, including part of an actin gene, part of a myosin heavy chain gene, and all of two myosin light chain genes, feminize chromosomal males. Both somatic and germline aspects of sex determination are affected. In contrast, about 40 kilobases of nematode autosomal DNA, phage lambda DNA, and plasmid pBR322 DNA do not affect sex determination. A feminizing region was localized to a maximum of 131 base pairs within an intron of the X-linked actin gene; a part of the gene that does not have this region is not feminizing. The results suggest that short, discrete elements found associated with many X-linked genes may act as signals for sex determination in C. elegans.
Actins↗