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)

Steroidogenic enzyme activities in the left ovary and the testes of 9- to 15-day-old chicken embryos were measured, and development of the activities was compared between sexes. Activity of delta 5-3 beta-hydroxysteroid dehydrogenase coupled with delta 5-delta 4 isomerase in the ovary and in the testis was comparable, and did not change throughout the period examined. Activity of 17 beta-hydroxysteroid dehydrogenase (17 beta-HSD) in the ovary was similar to or higher than that in the testis, depending on substrates employed. In both gonads, 17 beta-HSD activity did not change or tended to decrease from 9 to 15 days of development. On the other hand, activities of 17 alpha-hydroxylase, C-17--C-20 lyase in the ovary were three to eight times those in the testis, and aromatase activity in the ovary was definitely higher than that in the testis at all stages examined. The activities of 17 alpha-hydroxylase, C-17--C-20 lyase, and aromatase significantly increased from 9 to 11 days only in the ovary. From 13 to 15 days, the activities of 17 alpha-hydroxylase and C-17--C-20 lyase markedly increased only in the testis. These results suggest that, in the gonads of developing chicken embryos, there are sexual differences in the regulation of 17 alpha-hydroxylase, C-17--C-20 lyase, and aromatase activities.
Gen Comp Endocrinol 1988 Sep
PMID:Developmental changes of steroidogenic enzyme activities in the embryonic gonads of the chicken: the sexual difference. 284 54

Alterations of progesterone metabolism and especially of 20 alpha-hydroxysteroid dehydrogenase (20 alpha-HSD) activity were studied in cultured rat granulosa cells following various treatments. The cells were incubated for up to 48 h with or without follicle-stimulating hormone (FSH), androgens, hydroxyflutamide, estrogens, chlorea toxin, and dibutyryl cAMP [Bu2 cAMP]. Subsequently, the cells were incubated for 3 h with [4-14 C] progesterone (0.5 microM). The progesterone utilization and accumulation of 20 alpha-reduced and 5 alpha-reduced metabolites were assessed following thin-layer chromatography separation of radiolabeled steroids. Both FSH (1 microgram/ml) and testosterone (0.5 microM) decreased the 20 alpha-HSD activity by decreasing the maximal velocity (by 52% and 37%, respectively) without changing significantly the Km value. The inhibition of 20 alpha-HSD was demonstrable following 12 and 24 h exposure to FSH and following 24 and 48 h exposure to testosterone. Effects comparable to that induced by testosterone were elicited by other androgens (androstenedione and 5 alpha-dihydrotestosterone), but not by estrogens (estradiol-17 beta and estrone). Hydroxyflutamide reversed testosterone-induced effects: the increase of endogenous progesterone accumulation and the decrease of 20 alpha-HSD activity. Both cholera toxin (0.001-10 micrograms/ml) and Bu2 cAMP (62.5-1000 micrograms/ml) caused a dose-dependent inhibition of 20 alpha-HSD activity. Present results indicate that: the inhibition of 20 alpha-HSD by both FSH and androgens may be of a noncompetitive nature; androgen action on 20 alpha-HSD may be a true androgenic, receptor-mediated effect; and cAMP may mediate the FSH action on 20 alpha-HSD activity.
Biol Reprod 1985 Sep
PMID:Inhibition of 20 alpha-hydroxysteroid dehydrogenase activity by follicle-stimulating hormone and androgens in cultured rat granulosa cells: a search for the mechanism of action. 299 67

The sensitivity of soluble, 17 beta-hydroxysteroid dehydrogenase (17 beta-HSD) of human placenta to inactivation by fatty acids was examined. Exposure to the unsaturated fatty acids oleic, arachidonic, linoleic and linolenic acid resulted in the loss of activity. Methyl and ethyl esters of oleic acid, the saturated fatty acid, stearic acid and prostaglandins E2 and F2 alpha were without effect. Inactivation by oleic acid required the fatty acid at levels above its critical micelle concentration, 50 microM, as estimated by light-scattering. Steroid substrates and inhibitors did not protect against inactivation. NAD+, NADH, NADP+ and NADPH did protect. The concentrations of NADP+, 50 microM, and NAD, 1.5 mM, necessary for complete protection were significantly greater than their respective Michaelis constants, 0.16 microM and 15.2 microM. The data suggest that soluble 17 beta-HSD can bind to fatty acid micelles and that the binding site(s) on the enzyme are at or near pyridine nucleotide binding sites.
J Steroid Biochem 1985 Sep
PMID:Inactivation of soluble 17 beta-hydroxysteroid dehydrogenase of human placenta by fatty acids. 299 30

Three patients with idiopathic hyperaldosteronism were continuously treated with trilostane, a competitive inhibitor of adrenal 3 beta-hydroxysteroid dehydrogenase (3 beta-HSDH) (3 to 4 2/3 years). Trilostane, in conjunction with antihypertensive drugs, effectively decreased plasma aldosterone levels and improved hyperaldosteronism symptoms without undesirable side effects. Trilostane continued to be effective even when treatment was continuous. Rapid ACTH testing (iv bolus of 0.25 mg alpha 1-24 ACTH) was done on the day without trilostane after long-term treatment, and plasma levels of aldosterone and cortisol were compared to those obtained during a pre-treatment period. Results suggest that the inhibitory effect of trilostane on steroid biosynthesis rapidly disappears following discontinuance of trilostane administration even after long-term treatment, and that continuous treatment causes no significant or irreversible change in steroid biosynthesis. These results suggest that trilostane is a safe, feasible therapeutic agent for long-term treatment of idiopathic hyperaldosteronism.
Acta Endocrinol (Copenh) 1986 Sep
PMID:Long-term treatment of idiopathic hyperaldosteronism using trilostane. 302 Aug 49

Changes in the capacity of medaka, Oryzias latipes, ovarian follicles to convert exogenous 17 alpha-hydroxyprogesterone (17 alpha-OHprog) or testosterone to testosterone, estradiol-17 beta, and 17 alpha,20 beta-dihydroxy-4-pregnen-3-one (17 alpha,20 beta-diOHprog) were examined using 18-hr incubations. Under a constant long photoperiod (14 hr light-10 hr dark) at 26 degrees medaka spawn daily within 1 hr of the onset of light. Under these conditions, vitellogenesis and oocyte maturation of individual follicles occur within 72 hr, allowing accurate determination of the time of oocyte maturation and ovulation. In the absence of substrates, vitellogenic follicles isolated between 28 and 16 hr before spawning produced increased amounts of estradiol-17 beta, while postvitellogenic follicles between 14 and 8 hr produced a large amount of 17 alpha,20 beta-diOHprog. However, under the same conditions, testosterone levels were very low in follicles from all stages of development. The capacity of follicles to produce estradiol-17 beta in response to 17 alpha-OHprog or testosterone increased as follicles developed from the early to late vitellogenic stage, but declined during oocyte maturation. Maximum estradiol-17 beta production was observed in follicles at 20 hr before spawning. In contrast, the conversion of 17 alpha-OHprog to 17 alpha,20 beta-diOHprog was low in vitellogenic follicles and increased in follicles isolated immediately prior to or during oocyte maturation, with maximum 17 alpha,20 beta-diOHprog production occurring in follicles isolated at 14 hr before spawning. These results demonstrate a distinct shift in the activities of steroidogenic enzymes from C17-20 lyase, 17 beta-hydroxysteroid dehydrogenase (17 beta-HSD), and aromatase to 20 beta-hydroxysteroid dehydrogenase (20 beta-HSD) occurring in the medaka ovarian follicles immediately prior to oocyte maturation.
Gen Comp Endocrinol 1988 Sep
PMID:Influence of follicular development on steroid production in the medaka (Oryzias latipes) ovarian follicle in response to exogenous substrates. 319 72

The luteal function in newly inseminated female mice following exposure to alien males was investigated. The corpora lutea (CL) of newly inseminated females exhibited high delta 5 3 beta hydroxysteroid dehydrogenase (delta 5 3 beta HSD) activity at 24 hr or 48 hr (pro-oestrus) after the beginning of alien male exposure. By contrast, the enzyme activity in the CL at 72 hr (oestrus) after the beginning of alien male exposure was markedly less as compared with that in the CL of unexposed controls. This suggests that the CL of newly inseminated female mice can synthesise progesterone from its substrate at least up to 48 hr after the beginning of alien male exposure. Administration of prolactin to newly inseminated females beginning at 0 hr of alien male exposure prevented implantation failure; the majority of females showed implanted embryos. Prolactin administration starting at 24 hr after the beginning of alien male exposure was only partially effective, and that starting at 48 hr was totally ineffective in preventing implantation failure in newly inseminated females. The results indicate that the CL of newly inseminated females cease to respond to prolactin within 24 hr of alien male exposure, even though they exhibit the capacity to synthesise progesterone (as evidenced by the presence of delta 5 3 beta HSD activity) for a longer period.
Exp Clin Endocrinol 1988 Sep
PMID:The male-induced implantation failure (the Bruce effect) in laboratory mice: investigations on luteal failure in pregnancy-blocked females. 322 46

Sleep-induced narrowing of the upper airways underlies the widespread and supposedly trivial complaint of snoring, which may not only constitute a risk factor for the cardiocirculatory system, but in predisposed individuals may lead to the OSAS. The latter is a life-threatening condition characterized by repeated episodes of cessation of respiration at night with an associated drop in SaO2. Patients frequently present with hypersomnia, systemic and pulmonary hypertension, and even heart failure. HSD is the term we use to describe the evolutive stages from snoring to OSAS. ICAH, or Ondine's curse, is the clinical syndrome of sleep-related respiratory insufficiency in the absence of airway stenosis. We do not consider central sleep apnea to be an independent disorder. For the treatment of HSD, weight reduction should be attempted first. Also, if there are malformations in the upper airway, they should be surgically corrected. The use of various medications has been rather discouraging, and CPAP and other devices that are intended to overcome the obstruction are poorly tolerated by patients. The most effective surgical treatment for OSAS, even in progressed stages of the disease, is tracheostomy.
Semin Neurol 1987 Sep
PMID:Sleep-related respiratory disorders. 333 61

A method for the quantitative estimation of 11 beta-hydroxysteroid dehydrogenase activity (11 beta-HSD; EC.1.1.146) in human placental homogenates is described. This method is based on the separation of cortisol and cortisone by high performance liquid chromatography after extraction from homogenates incubated in the presence of cortisol and NADP. 11 beta-HSD activity (pmol/g wet weight per min) averaged 900 +/- 150 (mean +/- SEM) at 10 +/- 2 weeks of gestation, 915 +/- 35 at 17 +/- 2 weeks and 790 +/- 42 at 40 +/- 2 weeks, thus supporting the view that the placenta is an effective barrier to materno-fetal cortisol transfer throughout gestation.
Horm Metab Res 1986 Sep
PMID:11 beta-Hydroxysteroid dehydrogenase activity of the human placenta during pregnancy. 346 74

We recently identified that the Y' bile acid binders are 3 alpha-hydroxysteroid dehydrogenases (3 alpha-HSD). In the present studies, purified 3 alpha-HSD catalyzed rapid 3H loss from [3 beta-3H, C24-14C]lithocholic and chenodeoxycholic acids without net conversion to 3-oxo bile acids under physiologic pH and redox conditions. [3 beta-3H]Cholic acid was a poor substrate. The Y' fraction of hepatic cytosol was exclusively responsible for this activity and 3H was transferred selectively to NADP+. Time-dependent 3H loss was also seen in isolated hepatocytes. Further hydroxylation products of lithocholic and chenodeoxycholic acids lost 3H at the same rate, whereas 3H loss from lithocholic acid rapidly ceased, which suggests compartmentation of this bile acid in hepatocytes. Indomethacin inhibited 3H loss from bile acids either in incubations with the pure enzyme or in isolated hepatocytes. Indomethacin did not alter the initial uptake rate of bile acids by hepatocytes, but caused a redistribution of unconjugated bile acids into the medium at early time points (2.5 and 5.0 min) and that of conjugated bile acids at later time intervals (30 min). 3H loss from the 3 beta position therefore can be used to probe the interaction between bile acids and cytosolic 3 alpha-HSD in intact cells, and indomethacin is capable of inhibiting this interaction.
J Clin Invest 1987 Sep
PMID:Cyclical oxidation-reduction of the C3 position on bile acids catalyzed by rat hepatic 3 alpha-hydroxysteroid dehydrogenase. I. Studies with the purified enzyme, isolated rat hepatocytes, and inhibition by indomethacin. 347 98

The stimulatory effect of gonadotropins on steroid hormone production by the ovary is generally considered to be the result of an activation of the cholesterol side chain cleaving enzyme. The present study was undertaken to investigate whether the enzymic action of 3 beta-HSD and 20 alpha-HSD could be directly stimulated by hCG and/or PRL. Female immature rats were used. The ovaries were stimulated by PMSG injection to allow uniform growth of the follicles. The effect of hCG was evaluated both in in vivo and in vitro studies. The 3 beta-HSD activity in the ovarian tissue homogenate or dispersed cells was estimated from the rate of conversion of 14C-pregnenolone to 14C-progesterone in an in vitro incubation experiment. The activity of 20 alpha-HSD was measured by the conversion rate of 14C-progesterone to 14C-20 alpha-hydroxy-4-pregnen-3-one, hCG apparently stimulated the 3 beta-HSD activity both in vivo and in vitro. Under certain experimental conditions, PRL enhanced the stimulatory effect of hCG on 3 beta-HSD. Both hCG and PRL stimulated the 20 alpha-HSD activity. Intrinsic steroids, such as estrogens, androgens, and 20 alpha-hydroxy-4-pregnen-3-one, a major progestin in rodents, in the synthesis of steroid hormones was its inhibitory effect upon 3 beta-HSD.
Nihon Sanka Fujinka Gakkai Zasshi 1987 Sep
PMID:[Studies on the regulation of steroid biosynthesis in the rat ovary]. 347 2


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