Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:1.1.1.3 (HSD)
 3,464 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Many genes involved in gonadal development have been proposed for mammals. To elucidate if those genes play any critical role in sexual differentiation of the avian gonad, we have examined expressions of the genes for proposed sex-determining factors (SF1, Sox9, DMRT1, Wpkci, and AMH), steroidogenic enzymes (P-450scc, 3beta-HSD, P-450c17, 17beta-HSD and aromatase) and the estrogen receptor in the urogenital system during chicken embryogenesis (days 4-16 of incubation), using a semi-quantitative reverse transcription-polymerase chain reaction. Transcripts of the genes for sex-determining factors except Wpkci and AMH were detected in both sexes but had no sexual dimorphism. Wpkci expression was female specific and constantly high throughout incubation. AMH was expressed in both sexes from the earliest stages but was higher in males than in females after the onset of gonadal differentiation. Expressions of the genes for more downstream enzymes in a steroidogenic pathway, such as P-450c17, 17beta-HSD and aromatase, were clearly higher in females than in males. In particular, 17beta-HSD expression increased in the course of gonadal development in females, whereas it was constantly low in males. Aromatase was highly expressed in females during gonadal differentiation but not in males over the period. In addition, to elucidate the relationship between gene activation during embryogenesis and reproductive abnormalities in wild birds, we examined expressions of these genes in embryos treated with various doses of diethylstilbestrol (DES), as a representative estrogenic compound. DES had no effect on the expressions of all the genes in either sex during the periods of gonadal differentiation (days 8, 12, and 16). Sexual dimorphism of the gene expression for steroidogenic enzymes appeared to be closely related to gonadal development in the chicken embryo, especially in the female. However, all the genes examined here seem unlikely to respond to xenoestrogens.
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PMID:Gene expression of sex-determining factors and steroidogenic enzymes in the chicken embryo: influence of xenoestrogens. 1530 64

Environmental anti-androgens are increasingly being recognized as potential contributing factors in the chemically induced feminization of wild fish because, by blocking androgen action, they can produce phenotypic effects similar to environmental estrogens. The molecular mechanisms by which anti-androgens and estrogens exert feminizing effects, however, have not been systematically compared. Using a targeted approach, we profiled the expression responses of a suite of 22 genes involved in reproduction, growth and development (processes controlled by androgens and estrogens) in the liver and gonad in adult male and female fathead minnow (Pimephales promelas) exposed to the model anti-androgen flutamide and the model synthetic estrogen 17alpha-ethinylestradiol (EE(2)). Both flutamide (320 microg/L) and EE(2) (10ng/L) produced phenotypic effects indicative of feminization (induction of plasma vitellogenin, reduced gonadosomatic index, and reduced secondary sex characters), although for the chosen test concentrations EE(2) was the more potent. For the genes studied, flutamide and EE(2) produced distinct expression profiles, suggesting that they largely operate via distinct molecular mechanisms. As examples, in liver EE(2) (but not flutamide) exposure up-regulated estrogen receptor (ER) alpha mRNA, whereas flutamide exposure increased ERbeta and ERgamma mRNAs in males and resulted in decreased androgen receptor (AR) mRNA in females. In the testis, flutamide up-regulated genes coding for enzymes involved in androgen biosynthesis (cytochrome P450 17 [CYP17] and 11beta-hydroxysteroid dehydrogenase [11beta-HSD]) implying an inhibitory action on androgen negative feedback pathways. EE(2), in contrast, inhibited the expression of enzymes involved in androgen biosynthesis (CYP17, 11beta-HSD and 17beta-hydroxysteroid dehydrogenase [17beta-HSD]). There were also some commonalities in the molecular mechanisms of flutamide and EE(2) action, including the down-regulation of gonadal sex steroid receptor expression (gonadal AR and ovarian ERalpha), increased expression of genes coding for estrogen-producing enzymes (cytochrome P450 19A and B [CYP19A and CYP19B]), decreased expression of genes involved in testis differentiation (anti-Mullerian hormone [AMH] and doublesex and mab-3 related transcription factor 1 [DMRT1]), and decreased expression of hepatic genes which mediate wider physiological processes such as somatic growth (growth hormone [GH], GH receptor [GHR], insulin-like growth factor-I [IGF-I], IGF-I receptor [IGF-IR], thyroid hormone receptor alpha [TRalpha] and beta [TRbeta]).
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PMID:Gene expression profiles revealing the mechanisms of anti-androgen- and estrogen-induced feminization in fish. 1722 21