Showing papers on "Hydroxysteroid dehydrogenase published in 1985"
TL;DR: Examination of a variety of steroidal contraceptives as modulators of the dehydrogenase indicates that ethinylestradiol is a very poor inhibitor, while 6-medroxyprogesterone acetate (Provera) is an extremely potent inhibitor.
108 citations
TL;DR: The activity of 17β hydroxysteroid dehydrogenase (17OHSD) was measured in adipose tissue adjacent to benign or malignant breast tumours and was signficantly correlated with tumour size in malignant tumours but not with benign tumours.
Abstract: The activity of 17 beta hydroxysteroid dehydrogenase (170HSD) was measured in adipose tissue adjacent to benign or malignant breast tumours. 170HSD activity was significantly correlated with tumour size in malignant tumours (r = 0.75) but not with benign tumours (r = 0.28). Enzyme activity was reduced in adipose tissue adjacent to tumours obtained from inferior breast quadrants.
29 citations
TL;DR: 3β,17β‐Hydroxysteroid dehydrogenase (3β17/βHSDH) is an NAD‐dependent dehydrogen enzyme which has a double specificity for the 3‐ and 17‐positions on the steroid skeleton.
20 citations
Journal Article•
TL;DR: The presence of enzyme and hormones suggests that steroid hormone production takes place in very early preimplantation horse embryos.
Abstract: The activity of delta (5)3 beta-hydroxysteroid dehydrogenase was examined histochemically in 6 to 10 days aged horse blastocysts. A positive reaction was noted in the blastomeres of all embryos incubated in medium with substrate. Measurable amounts of progesterone, androgens and estrogens were found in blastocysts on day 8th. The presence of enzyme and hormones suggests that steroid hormone production takes place in very early preimplantation horse embryos.
20 citations
TL;DR: In this article, the authors propose a method to solve the problem of "uniformity" in the following manner, i.i.d. 0.3.3 0
Abstract: 3 0
19 citations
Journal Article•
TL;DR: It is suggested that ovarian estrogen is a natural inducer of rat liver 3α-hydroxysteroid:nicotinamide adenine dinucleotide (phosphate) oxidase reductase/ trans -1,2-dihydrobenzene-1, 2-diol dehydrogenase, suggesting that induction is responsible for the sex difference in enzyme activity.
Abstract: The 3 alpha-hydroxysteroid:nicotinamide adenine dinucleotide (phosphate) oxidoreductase (EC 1.1.1.50) of rat liver cytosol is indistinguishable from trans-1,2-dihydrobenzene-1,2-diol dehydrogenase (EC 1.3.1.20) (T.M. Penning, I. Mukharji, S. Barrows, and P. Talalay, Biochem. J., 222: 601-611, 1984) and has been implicated in the detoxification of ultimate carcinogens (H. R. Glatt et al., Science (Wash. DC), 215: 1507-1509, 1982). Using trans-1,2-dihydroxy-3,5-cyclohexadiene as a model substrate for trans-dihydrodiol proximate carcinogens, this study shows that the specific activity of 3 alpha-hydroxysteroid:nicotinamide adenine dinucleotide (phosphate) oxidoreductase is 2-fold higher in the 40-75% ammonium sulfate fraction prepared from female rat liver cytosol than in similar fractions prepared from males. Comparable differences were also observed for the nicotinamide adenine dinucleotide-dependent oxidation of 5 alpha-androstan-3 alpha-ol-17-one. Chromatofocusing of these cytosolic fractions separated the bulk of the protein from the dehydrogenase, which eluted as a single peak at pH 5.4. Examination of the protein profiles indicates that twice as much protein coeluted with the enzyme from female rat liver cytosol, suggesting that induction is responsible for the sex difference in enzyme activity. These differences were abolished by ovariectomy, while administration of a single dose of estradiol 3-sulfate (100 micrograms) to ovariectomized rats restored enzyme activity to within 90% of normal female levels. These findings suggest that ovarian estrogen is a natural inducer of rat liver 3 alpha-hydroxysteroid:nicotinamide adenine dinucleotide (phosphate) oxidase reductase/trans-1,2-dihydrobenzene-1,2-diol dehydrogenase.
17 citations
TL;DR: Only the enzymes specifically associated with follicular steroidogenesis were affected by administration of the drug, tetrahydrocannabinol.
Abstract: Using a microdensitometric histochemical assay, delta 5-3 beta-hydroxysteroid dehydrogenase activity and glucose-6-phosphate dehydrogenase Types I and II hydrogen generation were measured in preovulatory follicles from normal rats, and in follicles from rats given tetrahydrocannabinol for three days prior to sacrifice. Hydroxysteroid dehydrogenase and Type I hydrogen generation are involved in steroidogenesis, whereas Type II hydrogen generation is involved with general cellular metabolism. All ovaries were removed on pro-oestrus, frozen, sectioned and the sections reacted with the appropriate media. Enzyme activity was measured in the theca and in three regions of the membrana granulosa; peripheral, antral and corona radiata. Compared to control animals, the hydroxysteroid dehydrogenase activity was significantly reduced in all follicular regions in rats exposed to tetrahydrocannabinol. Type I hydrogen generation was significantly less in the theca and peripheral region of preovulatory follicles from rats given tetrahydrocannabinol, but the same in the antral region and corona radiata. In all follicular regions examined, Type II hydrogen generation was unchanged following tetrahydrocannabinol administration. Thus, only the enzymes specifically associated with follicular steroidogenesis were affected by administration of the drug.
5 citations
Journal Article•
5 citations
TL;DR: The effect of estradiol, hydrocortisone and progesterone on 3α,20β- and 3β,17β-hydroxysteroid dehydrogenase (HSD) in mutants of Streptomyces hydrogenans was compared to the steroid response of the wild type.
Abstract: The effect of estradiol, hydrocortisone and progesterone on 3α,20β-and 3β,17β-hydroxysteroid dehydrogenase (HSD) in mutants of Streptomyces hydrogenans was compared to the steroid response of the wild type. Mutants were defective in arginine biosynthesis and/or aerial mycelial formation and lacked both enzymes or only 17β-HSD. Some 17β-HSD mutants had lost the ability to be induced by estradiol, by progesterone or by both. Some 20β-HSD mutants had lost the ability to be induced by hydrocortisone, by progesterone or by both. Non-inducibility of 17β-and 20β-HSD by progesterone was not co-ordinate. An additional study of the growth phase-dependent enzyme activity of the wild type after induction with estradiol, hydrocortisone and progesterone was performed.
4 citations
TL;DR: Testosterone synthesis, demonstrated immunohistochemically, took place predominantly in the Leydig cells, but also to a small extent in the Sertoli cells.
Abstract: Gynecological, endocrinological and histological tests on a 19-year-old female patient led to the diagnosis of Sertoli-Leydig cell tumor (arrhenoblastoma) of intermediate differentiation. For enzyme h
3 citations
TL;DR: The kinetic properties of oestradiol 17 beta-dehydrogenase have been studied in the MCF-7 human breast cancer cell line and the enzyme was able to utilize both NAD and NADP as cofactors but at higher concentrations NAD was the more effective.
TL;DR: Rat ovarian 20α-hydroxysteroid dehydrogenase was shown to be effectively inhibited by adenosine derivatives, nicotinamide derivatives, NADP analogs, N -alkylammonium chlorides, and carboxylic acids through coenzyme-competitive inhibition studies.