Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:Q7LGC8 (HSD)
 3,196 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Testicular cholesterol side-chain cleavage enzyme (CSCCE) and delta5-3beta-hydroxysteroid dehydrogenase (delta5-3beta-HSD) activities were assessed 12 hours and 2, 4, 8, 16, and 32 days after surgical induction of bilateral cryptorchidism in adult rats. Within 12 hours after surgery CSCCE activity (expressed as dpm of isocaproic acid-14C formed from cholesterol-26-14C/3 hours/testis) was significantly reduced (P less than 0.01) in cryptorchid testes to approximately 55% of sham-operated control values and remained depressed at less than 50% of control activities 2, 4, 16, and 32 days after surgery. Cryptorchid testis delta5-3beta-HSD activity (measured by a pregnenolone substrate-depletion assay and expressed as mumoles of products/30 minutes/testis) did not differ from controls (P greater than 0.05) 1/2, 2, or 4 days after translocation of testes to the abdominal cavity. By day 8 of cryptorchidism, however, delta5-3beta-HSD activity was reduced to 60% of control values (P less than 0.05) and continued to decline to approximately 30% of controls during the remainder of the experimental period. These observed alterations in enzyme activities suggest an impairment in the ability of cryptorchid rat testes to synthesize androgens and further indicate that testicular CSCCE is more acutely sensitive to the cryptorchid milieu than delta5-3beta-HSD.
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PMID:Influence of experimental cryptorchidism on cholesterol side-chain cleavage enzyme and delta5-3beta-hydroxysteroid dehydrogenase activities in rat testes. 2 94

A partial testicular defect in testosterone secretion has been documented in a pubertal male with a congenital adrenal hyperplasia due to hereditary deficiency of the delta5-isomerase-3beta-hydroxysteroid dehydrogenase enzyme complex (delta5-3beta-HSD). Diagnosis of the enzymatic defect is based on the clinical picture of ambiguous genitalia and salt-losing crisis in infancy, together with high urinary delta5-pregnenetriol and plasma dehydroepiandrosterone when the patient was taken off replacement corticoid treatment. No hormonal response to ACTH or salt deprivation was demonstrable. In addition, in vivo studies revealed a partial enzymatic defect in the testis. Although plasma testosterone was low-normal (250 ng/100 ml), plasma delta5-androstenediol was markedly elevated and rose to a greater extent than testosterone after human chorionic gonadotropin administration. In vitro testicular incubation studies suggested a testicular delta5-3beta-HSD enzyme defect with less delta4 products formed from delta5 precursors than in a control testis. Histochemical studies of the testis were also consistent with this defect. Testicular biopsy revealed spermatogenic arrest, generally diminished Leydig cells, but with focal areas of Leydig cell hyperplasia as well as benign Leydig cell hyperplasia as well as benign Leudig cell nodules within the spermatic cord. In vivo studies of steroid metabolism suggested intact peripheral or hepatic delta5-3beta-HSD activity. These studies imply that delta5-3beta-HSD activity differs in the gonad, adrenal, and peripheral organs. These findings are compatible with the concept that the enzyme complex consists of subunits and/or that enzymes in these organs are under different genetic control.
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PMID:Persistent testicular delta5-isomerase-3beta-hydroxysteroid dehydrogenase (delta5-3beta-HSD) deficiency in the delta5-3beta-HSD form of congenital adrenal hyperplasia. 16 81

3beta-hydroxysteroid dehydrogenase and NADH-ferricyanide reductase activities were localized at the ultrastructural level in amphibian interrenal (adrenocortical) cells previously fixed in a mixture of formaldehyde and glutaraldehyde. Potassium ferricyanide was used as an electron acceptor. Copper ferrocyanide deposits resulting from 3beta-HSD activity were seen in close association with the external faces of the membranes of the smooth endoplasmic reticulum. Very rare grains of precipitate appeared in mitochondrial cristae. The addition of phenazine methosulfate to the incubation medium had no effect on these localizations. The interrenal cells showed also a strong NADH-ferricyanide reductase activity. The copper ferrocyanide grains were abundant in the mitochondrial cristae and in the hyaloplasm, where they were not preferentially associated with the smooth endoplasmic reticulum.
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PMID:Electron microscopic localization of 3beta-hydroxysteroid dehydrogenase and NADH-ferricyanide reductase activities in amphibian interrenal cells. 30 25

The effect of denervation on delta5-3beta-hydroxysteroid dehydrogenase (3beta-HSD) activity with pregnenolone as substrate was studied during pregnancy. The enzyme activity, that is interpreted as the capacity to secrete progesterone, was studied in both control and experimental pregnant rats. The ovaries of experimental rats were denervated 96 h prior to sacrifice. Denervation during early pregnancy did not affect 3beta-HSD activity in the interstitial gland (IG) and corpus luteum (CL). However, denervation resulted in decreased activity in both the IG and CL on days 10, 14 and 18. This reduced activity is interpreted as a decreased capacity of denervated ovaries to synthesize progesterone at this time in pregnancy.
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PMID:The effects of denervation on the localization of delta5-3beta-hydroxysteroid dehydrogenase activity in the rat ovary during pregnancy. 55 6

Aged (12- to 14-month-old) estrous and diestrous C57BL mice exhibited lower histochemically demonstrable ovarian delta5-3beta-hydroxysteroid dehydrogenase (3beta-HSD) activity in thecal, luteal, and interstitial cells, and lower (P less than 0.01) ovarian 3beta-HSD concentration and total content than did young (3-month-old) estrous animals. Administration of pregnant mare serum (PMS, 10 IU subcutaneously), followed in 40 hours by human chorionic gonadotropin (HCG, 5 IU subcutaneously) or HCG (2 IU daily for 4 days) alone, restored luteal and interstitial 3beta-HSD in aged mice. Follicular, lutea, and interstitial 3beta-HSD activity was increased in aged mice by a single PMS injection (10 IU). The total ovarian dehydrogenase concentration was increased 100% in aged animals by PMS and/or HCG administration. Restoration of histochemically demonstrable ovarian 3beta-HSD and total enzyme content in aged mice by PMS and/or HCG indicates ovarian sensitivity to gonadotropin and subnormal tropic hormone stimulation of the ovary in situ.
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PMID:Pregnant mare serum and human chorionic gonadotropin stimulate ovarian delta5-3beta-hydroxysteroid dehydrogenase in aged mice. 55 85

The enzymes delta5-3beta-hydroxysteroid dehydrogenase delta5-3beta-HSD) and glucose-6-phosphate dehydrogenase (G-6-PDH) were demonstrated histochemically in the adrenal cortex of female rat. The activities of these enzymes were increased significantly in the alloxan-treated rats kept in LD (light: darkness) cycles of 10:14 h. Continuous light exposure to diabetic animals appeared to decrease delta5-3beta-HSD and g-6-PDH in comparison to the diabetic rats kept in 10 h illumination. The evidence indicates that suppression of adrenal steroidogenesis in diabetic rats after exposure to continuous light is due to the alteration of pentose phosphate pathway.
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PMID:Adrenal dehydrogenases in alloxan diabetic rats following continuous exposure to light. 60 81

A simple procedure is described for solubilizing microsomal 3beta-hydroxysteroid dehydrogenase (3beta-HSD). Microsomes from rat adrenals or from testicular interstitial cells were incubated for 1 or 2 h at 0 C in a buffer containing NaCl followed by overnight storage at -20 C. Maximum solubilization of 3beta-hydroxy-5beta-androstan-17-one-HSD (androstane-3beta-HSD) was obtained by incubating adrenal microsomes with 1 M NaCl and interstitial cell microsomes with 2 M NaCl. Incubation with NaCl for 1 or 2 h resulted in maximum solubilization; incubation with NaCl for 4, 8 or 24 h did not change the amount of enzyme solubilized. From adrenal microsomes incubated with 1 M NaCl, up to 80% (105.7 millimicron/mg microsomes) of the total androstane-3beta-HSD activity was recovered in the supernatant following centrifugation at 130,000 x g for 1 h. The maximum amount of androstane-3beta-HSD solubilized from interstitial cell microsomes was 56% (29.5 millimicron/mg microsomes) at 2 M NaCl. The "solubilized" androstane-3beta-HSD was retarded when chromatographed on a Sephadex G-200 column and it did not pellet out when centrifuged at 130,000 x g for 15 h. KCL appeared to be equally effective in solubilizing androstane-3beta-HSD from microsomes. Other steroid dehydrogenase activities such as pregnanolone-HSD and 3beta-hydroxy-5alpha-androstan-17-one-HSD were also found in the 130,000 x g supernatant.
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PMID:A simple procedure for solubilizing 3beta-hydroxysteroid dehydrogenase from microsomes of rat adrenals and testis interstitial cells. 61 35

Abdominal vagotomy on Day 8 of pregnancy in rats decreased the number of live fetuses at Day 16 and increased the number of resorbing fetuses. The activity of delta5-3beta-hydroxysteroid dehydrogenase (3beta-HSD) in the corpus luteum and interstitial gland, LH and progesterone values in plasma and progesterone values in ovarian tissue were all lower in vagotomized rats than in sham-operated controls. Ovarian PGF levels were not affected. We suggest that these effects were caused by a direct effect of vagotomy on LH secretion which in turn lowers 3beta-HSD activity and progesterone levels in ovarian tissue and plasma, leading to fetal resorption.
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PMID:Effect of abdominal vagotomy of the pregnant rat on LH and progesterone concentrations and fetal resorption. 64 92

The activity of delta5-3beta-hydroxysteroid dehydrogenase (3beta-HSD) in the postovulatory follicle (POF) of the domestic hen was studied; it declined rapidly during the first 15 h after ovulation and then fell gradually until 52 h when there was no detectable activity. Comparison of 3beta-HSD and glucose 6-phosphate dehydrogenase activities in the theca and granulosa cells indicated that the changes in enzymatic activity can be attributed to the thecal component; the enzyme activity in granulosa cells was stable up to 35 h after ovulation. The results appear consistent with the hypothesis that the POF is a source of steroid hormones.
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PMID:Activity of 3beta-hydroxyteroid dehydrogenase in the postovulatory follicle of the domestic fowl (Gallus domesticus). 85 Feb 16

The ability of cultured midpregnancy mouse ovarian cells to synthesize progesterone de novo and from oxogenous pregnenolone has been assessed. The conversion of pregnenolone to progesterone is almost completely blocked by cyanoketone, a known inhibitor of delta5,3beta-hydroxysteroid dehydrogenase (3beta-HSD) activity, but is unaffected by aminoglutethimide, which inhibits the cholesterol side-chain cleavage enzyme complex (desmolase). Since there is little metabolism of the formed progesterone, the ability of ovarian cells to convert exogenous pregnenolone to progesterone in vitro reflects the activity of 3beta-HSD in these cells. Cultured ovarian cells are also capable of endogenous progesterone production in the absence of added pregnenolone, although the absolute amount of progesterone produced is considerably less than that produced from exogenous pregnenolone. Since endogenous progesterone accumulation is almost completely blocked by the addition of aminoglutethimide to the culture medium, it is concluded that this response does represent de novo progesterone synthesis. Neither bovine luteinizing hormone (LH) nor human chorionic gonadotrophin (hCG) affects 3beta-HSD activity in cultured ovarian cells. The ability of the cells to secrete or to further metabolize the progesterone formed is also unaffected. However, both LH and hCG stimulate endogenous progesterone production within one hour of their addition to the culture medium. The stimulation, 2-10 fold in several experiments, can be maintained for at least six days of culture, and is not a result of an increase in the growth rate of the ovarian cells. As would be expected, the stimulation is blocked by the addition of aminoglutethimide to the culture medium. Taken together, these facts suggest that gonadotrophic hormones stimulate progesterone production by ovarian cells specifically by their action at steps prior to the conversion of pregnenolone to progesterone.
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PMID:Gonadotrophin stimulation of progesterone synthesis by midpregnancy mouse ovarian cells in vitro. 95 70


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