Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: 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)

The adult Wistar strain albino rats were vasectomised by conventional method and maintained for six months. The vasectomized rat testis had elevated water content with depleted dry matter. Glycogen content was increased with indication of mobilization of hexoses into HMP pathway. The vasectomized rat testis showed preferential utilisation of triglycerides. In view of increased 3 beta-HSD and 17 beta-HSD activities, accelerated androgenesis was envisaged in vasectomized rat testis.
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PMID:Effect of bilateral vasectomy on testicular metabolism in albino rats. 657 6

An alternative approach to the regeneration of coenzymes is described here using immobilized microorganisms possessing "NADH-oxidase" function. Bacteria containing NADH-oxidase activity are immobilized by microencapsulation within artificial cells. In this form, the microencapsulated bacteria can recycle NADH back to NAD in the presence of molecular oxygen as an electron acceptor. The only byproduct of the recycling reaction is water. In order to perform the biological regeneration of NAD, the activity of NADH-oxidase was investigated in 13 strains of aerobic bacteria and yeast. The NADH-oxidizing bacteria Leuconostoc mesenteroides exhibited the highest activity among the microorganisms tested. The permeabilized bacteria showed 10% of their initial activity after microencapsulation. Light and electron microscopy studies of bacteria loaded microcapsules have been done. Enzymatic properties of microcapsule-immobilized bacteria were investigated in comparison with those of the free enzyme complex. Leuconostoc mesenteroides, containing NADH-oxidase, has been microencapsulated together with 3 alpha-hydroxysteroid dehydrogenase (3 alpha-HSDH) for stereospecific steroid oxidation. In a batch reactor, 2 mg of NAD, with recycling, allowed the same substrate consumption as 4.4 mg of NAD without recycling. The microencapsulated system can be used repeatedly. The system is functional for 10 h, during which time each molecule of NAD has been used 7.6 times.
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PMID:Selection and microencapsulation of an "NADH-oxidizing" bacterium and its use for NAD regeneration. 659 8

Human placental 20 alpha-hydroxysteroid dehydrogenase (20 alpha-HSDH) interconverts progesterone and 20 alpha-dihydroprogesterone (20 alpha-DHP). In this study, an endogenous inhibitor of the cytoplasmic 20 alpha-HSDH isolated from human term placenta is demonstrated. Characterization of the endogenous inhibitor was carried out by adding heat-denatured fractions of the 20 alpha-HSDH enzyme stock solution to the incubations. The aqueous phase of the 20 alpha-HSDH (after diethylether extraction) using 8-fold concentration of the enzyme inhibited the 20 alpha-HSDH activity by 50%. After ultrafiltration of the aqueous phase, this inhibitory effect (50%) was found in the aqueous fraction with a molecular weight above 12,800. No inhibition of the 20 alpha-HSDH was shown using the ether phase or the aqueous ultrafiltrate with a molecular weight below 12,800. The 20 alpha-HSDH was stimulated by human and bovine serum albumins up to 290% and 420% respectively. Bovine serum albumin showed a higher stimulatory effect on the oxidative (420%) than on the reductive (190%) pathway of the 20 alpha-HSDH. Ovalbumin and immunoglobulin G had no effect. The endogenous inhibitor of the cytoplasmic 20 alpha-HSDH isolated from the human term placenta is heat stable (100 degrees C), water soluble, not soluble in diethylether and has a molecular weight above 12,800. The stimulatory effect of serum albumins in 20 alpha-HSDH may be caused by binding and inactivation of the endogenous inhibitor.
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PMID:Endogenous inhibition of the 20 alpha-hydroxysteroid dehydrogenase (EC 1.1.1.149) in the human term placenta in vitro. 695 68

This study determined the effects of HSD administration on fluid distribution, following dehydration in Female Yucatan micro pigs. Dehydration at 33 degrees C resulted in: significantly increased core temperature (37.2 +/- 0.2 (mean +/- SE) to 39.0 +/- 0.1 degrees C), and decreased (4.4 +/- 0.4%) body weight and plasma volume (PV, 43 +/- 2 to 37 +/- 1 ml/kg). HSD but not saline administration resulted in significant increases (over postdehydration levels) in PV (46 +/- 3 ml/kg), sodium concentration (141 +/- 1 to 150 +/- 2 mEq/L), and osmolality (291 +/- 2 to 307 +/- 11 mOsm). Following return of water to the animals, these values returned to baseline levels. Since insensible (respiratory and transdermal) water loss for the 24 hr at 23 degrees C was 714 +/- 64 ml, and for the 24 hr at 33 degrees C was 653 +/- 64 ml, increasing the ambient temperature did not result in increased dehydration in swine. HSD administration restored PV to baseline levels despite prior water loss dehydration.
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PMID:Fluid shifts induced by the administration of 7.5% sodium chloride in 6% dextran 70 (HSD) in dehydrated swine. 750 27

Hyperthermia may be accompanied by dehydration with or without electrolyte loss. To determine the efficacy of hypertonic saline in dextran solution (HSD, 7.5% NaCl in 6% dextran 70) for the treatment of heat stroke, rats were deprived of water for 24 h (DE) or not (ND), and then they were heat-stressed, and 4 mL/kg of saline (SAL) or HSD was administered via jugular cannula at the end of heat stress (a core temperature of 42.3 degrees C). The following four groups of 10 rats (Wistar-Furth) were used: NDSAL, DESAL, NDHSD, and DEHSD. Four control groups not subjected to heat stress were also studied. Percent change in plasma volume (PV) from baseline was significantly decreased by DE vs. ND (-6.8 +/- 1.2 vs. +4.6 +/- 1.6%) and increased by HSD vs. SAL (+10.1 +/- 4.1 vs. -3.5 +/- 1.6%) administration. Rats that were DE had significantly higher heating rates and less water loss during heat than ND rats, but hydration status was not correlated to 24 h survival. HSD groups had significantly higher PV and survival rates than their corresponding SAL groups regardless of hydrational status.
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PMID:Treatment of hyperthermia and dehydration with hypertonic saline in dextran. 753 37

Two human choriocarcinoma cell lines, BeWo and Jar, were used as a model system to study 17 beta-hydroxysteroid dehydrogenase (17 beta-HSD) activity. Northern blot, Western blot and 3H-water assay were performed to investigate the mRNA species, protein and enzyme activity of 17 beta-HSD. Two sizes of 17 beta-HSD mRNA, 1.3 and 2.2 kb, were detected in BeWo and Jar cells. In BeWo cells the predominant mRNA species is 1.3 kb. Western blot analysis demonstrated high level of 17 beta-HSD immunoreactivity and the 3H-water assay demonstrated significant enzyme activity in BeWo cells. In contrast, in Jar cells, the predominant mRNA species is 2.2 kb. Jar cells contain very low 17 beta-HSD enzyme activity and Western blot failed to show detectable 17 beta-HSD immunoreactivity. It is possible that the 2.2-kb 17 beta-HSD mRNA cannot be efficiently translated into protein because of the presence of multiple AUGs and termination signals (UGAs, UAAs, and UAGs) at the 5'-untranslated and termination signals (UGAs, UAAs, and UAGs) at the 5'-untranslated region of the 2.2-kb mRNA.
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PMID:17 beta-Hydroxysteroid dehydrogenase: enzymatic activity and mRNA species in choriocarcinoma cells. 800 55

Corticotropin-releasing factor (CRF) has been reported to reduce food intake and body weight, and numerous studies suggest a role for CRF in putative mechanisms for the regulation of body energy. This study investigated the effects of ICV-administered antisense phosphorothioate oligonucleotides, directed against the CRF mRNA, on feeding behavior and body weight in rats. Sixteen male HSD rats were cannulated in the lateral ventricle, and given ad libitum access to tap water and a ground chow diet. Feeding behavior was recorded by computer, and meal patterns were assessed. Rats were given 3 micrograms each of two anti-CRF oligonucleotides (aCRF) or two control oligos in the hour before the onset of the nocturnal cycle for ten consecutive days. Cumulative food intake was assessed at 3, 6, 12 and 24 h after each injection, as well as over the 10-day injection period. Compared to missense controls, rats receiving the antisense oligonucleotides ate significantly more at 6 h (P = 0.01), but not at 3, 12, 24 h, or during the entire 10-day injection period (P > 0.05). There was no effect on body weight change, meal size, or meal interval (P > 0.05). These data indicate that daily administration of anti-CRF oligonucleotides has a significant short-term stimulatory effect on feeding behavior, but does not have a long-term effect on feeding or body weight gain.
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PMID:ICV administration of anti-corticotropin-releasing factor antisense oligonucleotide: effects on feeding behavior and body weight. 858 60

Rat liver 3 alpha-hydroxysteroid/dihydrodiol dehydrogenase (3 alpha-HSD) inactivates circulating steroid hormones and is involved in polycyclic aromatic hydrocarbon (PAH) carcinogenesis. It is the only HSD of known structure in the aldo-keto reductase (AKR) superfamily and may provide a paradigm for other mammalian HSDs in this family. The structure of the 3 alpha-HSD.NADP+ binary complex has been determined at 2.7 A resolution and refined to a crystallographic R-factor of 23.4% with good geometry. The model is similar to other binary complexes in the AKR superfamily in that NADP+ binds at the C-terminal end of an alpha/beta barrel. However, it is unique in that NADP+ is bound in two alternate conformations, probably because of the lack of a salt-linked "safety belt" over the pyrophosphate bridge. The structure supports a previously proposed catalytic mechanism for carbonyl reduction in which Tyr 55 is the general acid, and its effective pKa is lowered by the adjacent Lys 84. We present evidence that the structurally distinct short-chain dehydrogenase/reductase (SDR) superfamily may have convergently evolved a similar catalytic mechanism. Insight into substrate binding is offered by a crystal packing contact in which a neighboring molecule inserts a tryptophan residue (Trp 227) into an apolar cleft in 3 alpha-HSD. This cleft is proximal to the bound NADP+ cofactor and contains a surface of apolar residues (Leu 54, Trp 86, Leu 122, Phe 128, Phe 129, Leu 137, Phe 139), making it a likely candidate for the substrate-binding site. Thus, in forming this crystal contact, Trp 227 may mimic a portion of a bound steroid. In addition, we propose that a water molecule in the active site indicates the position of the hydroxyl oxygen in a 3 alpha-hydroxysteroid substrate. Knowledge of the position of this water molecule, combined with the stereochemistry of hydride transfer, suggests that the alpha face of a bound steroid will be oriented toward the side of the apolar cleft containing Trp 86.
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PMID:Structure of 3 alpha-hydroxysteroid/dihydrodiol dehydrogenase complexed with NADP+. 871 59

The theoretical efficacy of hypertonic saline (HS) resuscitation for hemorrhagic shock purportedly stems from the osmolar extraction of intracellular fluid into the plasma. This hypothesis presumes a concomitant expansion of the interstitial fluid space. Colloid resuscitation, in theory, expands the plasma volume by extracting interstitial fluid. These hypotheses were tested in a canine-modified Wigger's model of hemorrhagic shock. Forty, male, splenectomized dogs were anesthetized and instrumented. Animals underwent a baseline equilibration period followed by shock for 120 minutes. Each animal was randomized to one of four groups and received equal amounts of Na+ either as lactated Ringer's (LR) solution, 10% dextran 40 (Dex) in normal saline, 7.5% saline (HS), or 7.5% saline plus Dex (HSD). Parameters measured at baseline, shock, and at postresuscitation 30 minutes, 60 minutes, 90 minutes, and 120 minutes, included: mean pressure (MAP), output, pulmonary capillary wedge pressure, prenodal skin lymph flow, serum and lymph albumin, wet-to-dry skin ratios, and plasma volume. MAP, cardiac output, and plasma volume were most quickly restored with LR and Dex resuscitation (MAP = 106 and 118 mm Hg) compared to HS and HSD (MAP = 98 and 92 mm Hg). Lymph flow and lymph albumin flux were best restored with LR and HSD (mean = 85 and 48 microL/min) compared to Dex and HS (mean = 36 and 37 microL/min). Wet/dry skin ratios were greatest at 60 minutes in the LR group but similar at 120 minutes in all four groups. These data suggest that interstitial fluid space remains contracted during the first hour after HS, HSD, and Dex resuscitation compared with LR resuscitation, even though the restoration of plasma volume, MAP, and cardiac output is greatest with the Dex regimen. Further studies with total body water and intracellular water are needed in this model.
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PMID:Hemodynamic, plasma volume, and prenodal skin lymph responses to varied resuscitation regimens. 876 May 38

Although dehydration impairs the response to a fixed volume hemorrhage, both 7.5% hypertonic saline/6% dextran 70 (HSD: 4 mL/kg) and standard Ringer's lactate (33 mL/kg) are effective resuscitation fluids. However, the efficacy of resuscitation during continuing hemorrhage remains in question. Using a conscious swine model of continuous pressure-driven hemorrhage, we evaluated the effects of dehydration and HSD resuscitation on survival time, hemorrhage volume, regional blood flows, and central hemodynamics. Three groups of pigs were compared: euhydrated control (EC), dehydrated control (48 h water deprived) (DC); and dehydrated and resuscitated with HSD (D + HSD). All pigs were subjected to an initial 37% blood volume hemorrhage for 60 min followed by a continuous hemorrhage proportional to the instantaneous mean arterial pressure. The D + HSD pigs were resuscitated at the end of the 37% blood volume hemorrhage. Dehydration reduced body weight (-6.5 +/- .3%) and increased hematocrit (8.9 +/- 1.8%), serum osmolality (11.6 +/- .9%), serum sodium (11.9 +/- .9%), and serum total protein (9.4 +/- 1.8%). Compared with the EC group, DC had a greater increase in heart rate and arterial base deficit in response to the pressure-driven hemorrhage and a reduced pH and survival time (159 vs. 107 min). In contrast to the DC group, D + HSD had increased mean arterial pressure, cardiac output, oxygen delivery, and regional blood flows to the gut (superior mesenteric artery), kidneys, liver (hepatic artery), and adrenals at 5 min after HSD resuscitation. The HSD did not increase blood loss but tended to prolong survival (+26 min; p = .1079). thus, dehydration compromises survival time (-33%) and the hemodynamic and metabolic responses to pressure-driven hemorrhage, while treatment with HSD improves the hemodynamic responses.
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PMID:Hypertonic saline/dextran treatment for severe pressure-driven hemorrhage in dehydrated conscious swine. 890 50


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