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Hydroxysteroid dehydrogenase

About: Hydroxysteroid dehydrogenase is a research topic. Over the lifetime, 1087 publications have been published within this topic receiving 28468 citations. The topic is also known as: hydroxysteroid dehydrogenase.


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Journal ArticleDOI
TL;DR: The results indicate that steroid dehydrogenase which utilizes NADP + for the transfer of electrons is not influenced by adenosine 3',5'-cyclic-monophosphoric acid, and confirms early reports on the inhibitory effect of this nucleotide.

5 citations

Journal ArticleDOI
TL;DR: Luteolysis was induced in rats during late pregnancy by fetoplacental removal, and was monitored by the increased activity of luteal 20 alpha-hydroxysteroid dehydrogenase (20 alpha-OHSDH), which was more readily induced on day 19 than on day 18.
Abstract: Luteolysis was induced in rats during late pregnancy by fetoplacental removal, and was monitored by the increased activity of luteal 20 alpha-hydroxysteroid dehydrogenase (20 alpha-OHSDH) The extent of enzyme induction over a given length of time varied according to the time of day at which the fetuses and placentae were removed, 1100 and 2100 h appearing to give optimal and minimal enzyme activities respectively The 20 alpha-OHSDH was more readily induced on day 19 than on day 18

5 citations

Journal ArticleDOI
TL;DR: It is suggested that 17β-HSD2 plays a crucial role in almost all tissues protecting against excessive levels of active steroid hormone, and GI tract maybe an important steroid hormone metabolizing organ in Hu-Sheep.
Abstract: 17β-Hydroxysteroid dehydrogenase type 2 (17β-HSD2) catalyzes the NADP+-dependent oxidation of the most potent estrogen 17β-estradiol into the weak estrogen estrone, and the conversion of testosterone to androstenedione. It has been reported that 17β-HSD2 was expressed in many tissues in human, rats, however, the full-length sequence of 17β-HSD2 gene and its expression in ewe were still unknown. In this study, we cloned the full-length cDNA sequence and investigated mRNA differential expression in 28 tissues of 12 adult Hu-Sheep which were fed with high- and low- dietary intake. The 1,317 bp full-length cDNA sequence was first cloned. The coding region was 1,167 bp in length, and the monomer was estimated to contain 389 amino acid residues. It shares high AA sequence identity with that of bos Taurus (96.13 %), sus scrofa (77.06 %), canis lupus familiaris (70.44 %), Callithrix jacchus (65.72 %), Nomascus leucogenys (65.46 %), pan troglodytes (65.21 %), human (64.69 %), mus musculus (58.35 %), and a comparatively lower identity to danio rerio (37.85 %). 17β-HSD2 gene was high expressed in gastrointestinal (GI) tract, liver, but weakly expressed in other tissues. No detected expression was examined in lung. 17β-HSD2 gene expression was significantly difference in rumen, omasum, duodenum, cecum, hypophysis after high- and low- dietary intake. Results from the present study suggested that 17β-HSD2 plays a crucial role in almost all tissues protecting against excessive levels of active steroid hormone, and GI tract maybe an important steroid hormone metabolizing organ in Hu-Sheep. This present study is the first to provide the primary foundation for further insight into this ovine gene.

5 citations

Journal ArticleDOI
TL;DR: The results suggested that the metabolic ability of 20alpha-hydroxyprogesterone in mouse oocytes increases during maturation, but the change in the metabolic able of such a steroid is not related to nuclear maturation.
Abstract: The activities of hydroxysteroid dehydrogenases (HSDs) were histochemically demonstrated in mouse oocytes in the process of maturation in vivo and in vitro, and the changes in steroid metabolism during meiotic maturation and also the relationship between nuclear maturation and changes in steroid metabolism in the cytoplasm were examined. In mouse oocytes 0 h after human chorionic gonadotrophin (hCG) injection, the activities of Δ5-3β-HSD (with DHA, pregnenolone and 17α-hydroxypregnenolone as the substrates), 17β-HSD (estradiol-17β and testosterone) and 20β-HSD (17α-hydroxyprogesterone and 20β-hydroxyprogesterone) were observed in 87 to 97% of those, but that of 20α-HSD (20α-hydroxyprogesterone) was not. The percentages of oocytes showing the activities of Δ5-3β-HSD, 17β-HSD and 20β-HSD did not change during maturation in vivo or in vitro. Oocytes with 20α-HSD activity appeared 4 h after the hCG injection or after culture for 4 h and the rates of those reached 92 and 100%, respectively, 14 h after the hCG injection or after culture for 14 h. In oocytes cultured for 8 h with olomoucine or 3-isobutyl-1-methylxanthine, nuclei were almost all in the germinal vesicle stage, and activity of 20α-HSD was observed in 84 and 89% of the treated oocytes, respectively. On the other hand, 81% of control oocytes showed 20α-HSD activity, with no significant difference from the rate for the olomoucine- or 3-isobutyl-1-methylxanthine-treated oocytes. The present findings suggested that the metabolic abilities of progesterone, 17α-hydroxyprogesterone, 17α,20β-dihydroxyprogesterone, 20β-hydroxyprogesterone, androgen and estradiol-17β in the cytoplasm are constantly present in mouse oocytes in the process of maturation in vivo and in vitro. The results also suggested that the metabolic ability of 20α-hydroxyprogesterone in mouse oocytes increases during maturation, but the change in the metabolic ability of such a steroid is not related to nuclear maturation.

5 citations

Journal ArticleDOI
TL;DR: It is suggested that inactivation of the testicular dehydrogenase system leads to insufficient endogenous Δ4,3-ketoandrogen (testosterone) production, thus allowing the development of the nipple in the male, and in female fetuses the analog inhibits nipple development.
Abstract: Summary The development of mammary glands has been studied in fetuses of pregnant rats treated with an analog (2α-cyano-4, 4,17α-trimethyl-androst-5-en-17β3-ol-3-one) of a C-19 substrate of 3β-hydroxysteroid dehydrogenase and Δ5-4, 3-ketosteroid isomerase, which is a selective inhibitor of these enzymes. In male fetuses, the analog causes the development of nipples, which are normally suppressed by fetal testicular function. In light of the previous demonstration of the feminizing effect of the analog on the male external genitalia due to inhibition of the fetal testicular dehydrogenase, this observation suggests that inactivation of the testicular dehydrogenase system leads to insufficient endogenous Δ4,3-ketoandrogen (testosterone) production, thus allowing the development of the nipple in the male. In female fetuses, the analog inhibits nipple development, probably because of adrenal overproduction of 3β-hydroxyandrogens in response to inhibition of the adrenal dehydrogenase system. The authors are grateful for the excellent technical assistance of Miss Esther Levy, Mrs. Gwendolyn Peyton, and Mrs. Barbara Sperling.

5 citations


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Performance
Metrics
No. of papers in the topic in previous years
YearPapers
202319
202217
20218
202016
201916
20186