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)

Activities of delta 5-3 beta-hydroxysteroid dehydrogenase (3 beta-HSDH) and 17 beta-hydroxysteroid dehydrogenase (17 beta-HSDH)) were histochemically demonstrated in the alveoli of the uropygial glands of male domestic pigeons (Columba livia Gmelin). The level of 3 beta-HSDH (Substrates: pregnenolone and dehydroepiandrosterone) was very low. On the other hand, an intense activity of 17 beta-HSDH was observed in the glandular alveoli of both sexually immature and adult pigeons when testosterone was used as the substrate. In the adult specimens, bilateral castration resulted in a moderate increase of the level of 17 beta-HSDH indicating a faster rate of conversion of testosterone into the weaker androgen, namely, delta 4-androstene-3,17-dione. On the other hand, administration of testosterone propionate (TP), 500 micrograms/bird/day for 15 days in the intact prepubertal and castrated adult pigeons caused a perceptible depletion of 17 beta-HSDH, which may be correlated with the increase in the local concentration of testosterone. Low dose of TP (100 micrograms/day) had no effect. When estradiol-17 beta was used as the substrate for 17 beta-HSDH, there was only a feeble response within the alveoli.
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PMID:Alteration in the histochemical profile of steroid dehydrogenases in the uropygial gland of male domestic pigeons following androgen deprivation and testosterone supplement. 347 85

The enzyme 17 beta-hydroxysteroid dehydrogenase (17 beta-HSD) has been shown to exist biochemically and histochemically in the toad testis. A single injection of cadmium chloride (0.5 mg/toad) resulted 7 days later in reduced 17 beta-HSD activity in the testis and decreased serum testosterone with an increase in thumb pad glycogen content. It is concluded that cadmium induced changes lead to inhibition of androgen synthesis in the toad testis.
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PMID:Effect of cadmium on 17 beta-hydroxysteroid dehydrogenase in toad testis. 347 11

Immunocytochemical localization of 17 beta-hydroxysteroid dehydrogenase (17 beta-HSD) and its relation to the ultrastructure of steroidogenic cells were examined in mature and immature rat ovaries. In mature (8-10 weeks old) rat ovaries, the theca interna cells of secondary as well as Graafian follicles, and the interstitial gland cells were all strongly stained with anti-17 beta-HSD antibody. However, granulosa cells, corpus luteum cells, oocytes and peritoneal epithelial cells were negative against this staining. In the ovaries of 1-week-old rats, all these cells were negative to immunostaining for 17 beta-HSD. In the ovaries of 2-week-old rats, the theca interna cells of secondary follicles and the interstitial gland cells showed a positive reaction for the 17 beta-HSD activity. Electron microscopic examination demonstrated the presence of characteristic structures for steroid secretory cells such as many lipid droplets, well developed smooth endoplasmic reticulum, and oval mitochondria with tubular cristae in the theca interna cell of secondary as well as Graafian follicles and in the interstitial gland cell of mature rat ovaries. In the ovaries of 1-week-old rats, all the theca cells of the primary and secondary follicles were fibroblast-like in their shape and fine structure, and typical interstitial cells were not recognized. In the 2-week-old rats, some of the theca interna cells and interstitial cells were well differentiated in ultrastructure, showing characteristic features for steroid secretory cells. These findings indicate that by 2 weeks after birth, theca interna cells and interstitial gland cells acquire the ability for testosterone production as seen in mature rat ovaries.
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PMID:Immunocytochemical localization of 17 beta-hydroxysteroid dehydrogenase (17 beta-HSD), and its relation to the ultrastructure of steroidogenic cells in immature and mature rat ovaries. 348 42

The 17 beta-hydroxysteroid dehydrogenase (17 beta-HSD) activity in rat and mouse preimplantation embryos was determined by measuring the interconversion of estradiol (E2) and estrone (E1). Rat and mouse embryos were cultured in medium containing 450 nM [3H]E1 or -E2 and the amount of [3H]E1 and -E2 in the medium at the end of the first hour was determined. The results showed that in both species 17 beta-HSD activity was detectable from the one-cell stage (Day 1) onward. In the rat, 17 beta-HSD effected primarily E2----E1 conversion, with the activity decreasing from Day 1 to Day 5. In the mouse, we found primarily E1----E2 conversion from Day 1 to the morning of Day 4, then E2----E1 increased sharply to near the E1----E2 rate in the evening of Day 4 and surpassed the E1----E2 rate the next morning. It seems that: 1) 17 beta-HSD is active throughout the entire preimplantation period, and 2) the enzyme activity changes during preimplantation development. Thus, the rat and mouse preimplantation embryo could regulate the E1- to -E2 ratio in the embryos and in their environment.
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PMID:Changing 17 beta-hydroxysteroid dehydrogenase activity in preimplantation rat and mouse embryos. 385 41

During storage at 4 degrees C, the 17 beta-hydroxysteroid dehydrogenase activity of human placental microsomes with estradiol-17 beta was more stable than that with testosterone. In order to evaluate the basis for this difference, kinetics with C18-, C19-, and C21- steroids as substrates and/or inhibitors was studied in conjunction with an analysis of the effects of detergents. Both 17 beta-hydroxysteroid dehydrogenase (17 beta-HSD) and 20 alpha-hydroxysteroid dehydrogenase (20 alpha-HSD) activities were detected. At pH 9.0, apparent Michaelis constants were 0.8, 1.3, and 2.3 microM for estradiol-17 beta, testosterone, and 20 alpha-dihydroprogesterone, respectively, 17 beta-HSD activity with testosterone was inhibited by estradiol-17 beta, 5 alpha-dihydrotestosterone, 5 beta-dihydrotestosterone, 20 alpha-dihydroprogesterone, and progesterone. In each case 90 to 100% inhibition was observed at 50 to 200 microM steroid. Activity with 20 alpha-dihydroprogesterone was similarly sensitive to inhibition by C19-steroids. By contrast, 25 to 45% of the activity with estradiol-17 beta was not inhibited by high concentrations of C19- or C21-steroids and differed from the 17 beta-HSD activity with testosterone and the major fraction of that with estradiol-17 beta by being insensitive to solubilization by detergent. These results are consistent with an association of two dehydrogenase activities with human placental microsomes. One recognizes C18-, C19-, and C21-steroids as substrates with comparable affinities. The second appears to be highly specific for estradiol-17 beta. The former activity may account for most if not all of the oxidation-reduction at C-17 of C19-steroids and at C-20 of C21-compounds at physiological concentrations by term placental tissue.
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PMID:17 beta-hydroxysteroid and 20 alpha-hydroxysteroid dehydrogenase activities of human placental microsomes: kinetic evidence for two enzymes differing in substrate specificity. 385 47

Concentrations of cytosol estrogen (ERc) and progestin (PRc) receptors and the activities of 17 beta-hydroxysteroid dehydrogenase (17-HSD) were measured in 80 untreated and 23 danazol-treated endometriotic tissue specimens. The results were compared with those obtained from endometrium specimens prior to or following danazol or medroxyprogesterone acetate (MPA) treatment. The concentrations of ERc and PRc in the endometriotic tissue were lower than corresponding values in the endometrium. Cytosol female sex steroid receptors were always present in the normal endometrium, whereas only 70% of the endometriotic lesions were simultaneously ERc- PRc-positive (receptor concentration greater than or equal to 3 and greater than or equal to 6 fmol/mg cytosol protein respectively), 24% PRc-positive, and 6% receptor-negative. In the endometriotic tissue, the mean concentrations of PRc during the luteal phase of the cycle (90 +/- 23, SE, fmol/mg protein) were lower (p less than 0.05) than during the follicular phase (177 +/- 32 fmol/mg protein), while the ERc concentrations and 17-HSD activities did not show any cyclic variations. Danazol and MPA had similar effects on the endometrium, both inducing a decrease in concentration of the female sex steroid receptors and an increase in activity of 17-HSD during short-term treatment (one week), and a decrease in activity of the enzyme during long-term treatment (3 weeks). The effect of danazol on the endometriotic tissue differed from that found in the endometrium. Danazol did not alter the activity of 17-HSD or the concentration of PRc but tended to increase the concentration of ERc in endometriotic tissue when given for 7-30 days.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Cytosol estrogen and progestin receptor concentrations and 17 beta-hydroxysteroid dehydrogenase activities in the endometrium and endometriotic tissue. Effects of hormonal treatment. 609 22

Adult male rats were given injections of oestradiol-17 beta (50 micrograms/100 g body wt per day) for 7 days. When they were killed 14 days after the last injection, serum levels of gonadotrophins and testosterone and weights of accessory sex organs were less, testicular 17 beta-hydroxysteroid dehydrogenase (17 beta-HSD) activity was suppressed and spermatogenesis was inhibited. Administration of alpha 2u-globulin (1.5 mg/day) for 14 days to oestrogen-treated rats and for 10 days to control rats resulted in increased concentrations of gonadotrophins and testosterone in the serum. Accessory sex organ weight and spermatogenesis appeared to be normal while 17 beta-HSD activity increased in oestrogen-treated rats after treatment with alpha 2u-globulin. It was concluded that alpha 2u-globulin has an effect on testicular function in oestrogenized rats by inducing gonadotrophin and testosterone synthesis.
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PMID:Effect of alpha 2u-globulin on serum concentration of gonadotrophins and testicular activity in oestrogen-treated rats. 618 60

Adult male rats were treated with estradiol-17 beta (50 micrograms/100 g body wt./day) for 7 days. When the animals were killed 14 days later, the levels of serum gonadotrophins, testosterone and alpha 2u-Globulin as well as the weight of sex organs were reduced, testicular 17 beta-hydroxysteroid dehydrogenase (17 beta-HSD) activity was also suppressed; spermatogenesis was inhibited. Administration of corticosterone (2 mg/day) for 14 days to estrogen-treated rats increased the concentration of gonadotrophins, testosterone and alpha 2u-globulin in the serum. The weight of accessory sex organs and spermatogenesis appeared to be normal while 17 beta-HSD activity increased in estrogen-treated rats after treatment with corticosterone. It is concluded that corticosterone has an effect on testicular function by inducing alpha 2u-globulin and gonadotrophins in estrogen treated rats.
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PMID:Studies on the effect of corticosterone treatment on testicular activity, serum concentration of gonadotrophins, testosterone and alpha 2 u-globulin in rats pre-treated with estrogen. 620 16

The presence and distribution of delta 5-3 beta-hydroxysteroid dehydrogenase (delta 5-3 beta-HSD: EC 1.1.1.51) and 17 beta-hydroxysteroid dehydrogenase (17 beta-HSD: EC 1.1.1.51) were studied histochemically in the excurrent ducts of the rabbit, hamster and marmoset monkey. Dehydroepiandrosterone (DHEA) and testosterone were used as substrates for delta 5-3 beta-HSD and 17 beta-HSD respectively, while phenanthroline monohydrate was used to eliminate non-specific staining due to other tissue dehydrogenases. The rabbit possessed least enzyme activity, which was confined to tubules in the middle segment of the epididymis. Enzyme activity was demonstrable throughout the excurrent ducts of the hamster and marmoset, with maximal staining occurring in the middle segment of the epididymis in both species. The region of maximum activity of hydroxysteroid dehydrogenase is where spermatozoa first develop their fertilizing capacity.
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PMID:Localization of delta 5-3 beta- and 17 beta-hydroxysteroid dehydrogenase activity in the efferent ducts, epididymis and vas deferens of the rabbit, hamster and marmoset monkey. 621 28

Concentrations of ADIOL, DHA and DHAS were measured in human breast tumours and normal tissue from the same breast and related to 17 beta-hydroxysteroid dehydrogenase (17 beta HSD) activity in these tissues. ADIOL and DHA were significantly higher in tumour tissue compared to normal tissue from the same breast (paired t-test: P less than 0.05 and P less than 0.01 respectively) whereas the difference between concentrations of DHAS in normal tissue and tumour tissue was not significant. There was a positive correlation between ADIOL and DHA in both tissues (P less than 0.001) but for DHAS the relationship was only significant in normal tissue (ADIOL:DHAS, P less than 0.001; DHA:DHAS, P less than 0.002). An increase in 17 beta-HSD activity was associated with an increase in DHAS concentrations in both normal and tumour tissue (P less than 0.01 and P less than 0.001 respectively) and with an increase in DHA concentrations in normal tissue (P less than 0.05). These results might be explained by an impairment in the balance between sulphatase and sulphotransferase activity in breast tumours.
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PMID:Adrenal androgen concentrations in breast tumours and in normal breast tissue. The relationship to oestradiol metabolism. 623 24


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