Hydroxysteroid Dehydrogenases: Enzymes of the oxidoreductase class that catalyze the dehydrogenation of hydroxysteroids. (From Enzyme Nomenclature, 1992) EC 1.1.-.3-Hydroxysteroid Dehydrogenases: Catalyze the oxidation of 3-hydroxysteroids to 3-ketosteroids.17-Hydroxysteroid Dehydrogenases: A class of enzymes that catalyzes the oxidation of 17-hydroxysteroids to 17-ketosteroids. EC 1.1.-.20-Hydroxysteroid Dehydrogenases: A group of enzymes that catalyze the reversible reduction-oxidation reaction of 20-hydroxysteroids, such as from a 20-ketosteroid to a 20-alpha-hydroxysteroid (EC 1.1.1.149) or to a 20-beta-hydroxysteroid (EC 1.1.1.53).3-alpha-Hydroxysteroid Dehydrogenase (B-Specific): A 3-hydroxysteroid dehydrogenase which catalyzes the reversible reduction of the active androgen, DIHYDROTESTOSTERONE to 5 ALPHA-ANDROSTANE-3 ALPHA,17 BETA-DIOL. It also has activity towards other 3-alpha-hydroxysteroids and on 9-, 11- and 15- hydroxyprostaglandins. The enzyme is B-specific in reference to the orientation of reduced NAD or NADPH.11-beta-Hydroxysteroid Dehydrogenase Type 2: An high-affinity, NAD-dependent 11-beta-hydroxysteroid dehydrogenase that acts unidirectionally to catalyze the dehydrogenation of CORTISOL to CORTISONE. It is found predominantly in mineralocorticoid target tissues such as the KIDNEY; COLON; SWEAT GLANDS; and the PLACENTA. Absence of the enzyme leads to a fatal form of childhood hypertension termed, APPARENT MINERALOCORTICOID EXCESS SYNDROME.11-beta-Hydroxysteroid Dehydrogenase Type 1: A low-affinity 11 beta-hydroxysteroid dehydrogenase found in a variety of tissues, most notably in LIVER; LUNG; ADIPOSE TISSUE; vascular tissue; OVARY; and the CENTRAL NERVOUS SYSTEM. The enzyme acts reversibly and can use either NAD or NADP as cofactors.11-beta-Hydroxysteroid Dehydrogenases: Hydroxysteroid dehydrogenases that catalyzes the reversible conversion of CORTISOL to the inactive metabolite CORTISONE. Enzymes in this class can utilize either NAD or NADP as cofactors.Estradiol Dehydrogenases: Enzymes that catalyze the oxidation of estradiol at the 17-hydroxyl group in the presence of NAD+ or NADP+ to yield estrone and NADH or NADPH. The 17-hydroxyl group can be in the alpha- or beta-configuration. EC 1.1.1.62Sulfotransferases: Enzymes which transfer sulfate groups to various acceptor molecules. They are involved in posttranslational sulfation of proteins and sulfate conjugation of exogenous chemicals and bile acids. EC 2.8.2.Cortisone: A naturally occurring glucocorticoid. It has been used in replacement therapy for adrenal insufficiency and as an anti-inflammatory agent. Cortisone itself is inactive. It is converted in the liver to the active metabolite HYDROCORTISONE. (From Martindale, The Extra Pharmacopoeia, 30th ed, p726)Steroid 17-alpha-Hydroxylase: A microsomal cytochrome P450 enzyme that catalyzes the 17-alpha-hydroxylation of progesterone or pregnenolone and subsequent cleavage of the residual two carbons at C17 in the presence of molecular oxygen and NADPH-FERRIHEMOPROTEIN REDUCTASE. This enzyme, encoded by CYP17 gene, generates precursors for glucocorticoid, androgen, and estrogen synthesis. Defects in CYP17 gene cause congenital adrenal hyperplasia (ADRENAL HYPERPLASIA, CONGENITAL) and abnormal sexual differentiation.Alcohol Oxidoreductases: A subclass of enzymes which includes all dehydrogenases acting on primary and secondary alcohols as well as hemiacetals. They are further classified according to the acceptor which can be NAD+ or NADP+ (subclass 1.1.1), cytochrome (1.1.2), oxygen (1.1.3), quinone (1.1.5), or another acceptor (1.1.99).Steroids: A group of polycyclic compounds closely related biochemically to TERPENES. They include cholesterol, numerous hormones, precursors of certain vitamins, bile acids, alcohols (STEROLS), and certain natural drugs and poisons. Steroids have a common nucleus, a fused, reduced 17-carbon atom ring system, cyclopentanoperhydrophenanthrene. Most steroids also have two methyl groups and an aliphatic side-chain attached to the nucleus. (From Hawley's Condensed Chemical Dictionary, 11th ed)NAD: A coenzyme composed of ribosylnicotinamide 5'-diphosphate coupled to adenosine 5'-phosphate by pyrophosphate linkage. It is found widely in nature and is involved in numerous enzymatic reactions in which it serves as an electron carrier by being alternately oxidized (NAD+) and reduced (NADH). (Dorland, 27th ed)Hydrocortisone: The main glucocorticoid secreted by the ADRENAL CORTEX. Its synthetic counterpart is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions.L-Lactate Dehydrogenase: A tetrameric enzyme that, along with the coenzyme NAD+, catalyzes the interconversion of LACTATE and PYRUVATE. In vertebrates, genes for three different subunits (LDH-A, LDH-B and LDH-C) exist.Testosterone: A potent androgenic steroid and major product secreted by the LEYDIG CELLS of the TESTIS. Its production is stimulated by LUTEINIZING HORMONE from the PITUITARY GLAND. In turn, testosterone exerts feedback control of the pituitary LH and FSH secretion. Depending on the tissues, testosterone can be further converted to DIHYDROTESTOSTERONE or ESTRADIOL.Kinetics: The rate dynamics in chemical or physical systems.Androsterone: A metabolite of TESTOSTERONE or ANDROSTENEDIONE with a 3-alpha-hydroxyl group and without the double bond. The 3-beta hydroxyl isomer is epiandrosterone.Liver: A large lobed glandular organ in the abdomen of vertebrates that is responsible for detoxification, metabolism, synthesis and storage of various substances.Alcohol Dehydrogenase: A zinc-containing enzyme which oxidizes primary and secondary alcohols or hemiacetals in the presence of NAD. In alcoholic fermentation, it catalyzes the final step of reducing an aldehyde to an alcohol in the presence of NADH and hydrogen.Glyceraldehyde-3-Phosphate Dehydrogenases: Enzymes that catalyze the dehydrogenation of GLYCERALDEHYDE 3-PHOSPHATE. Several types of glyceraldehyde-3-phosphate-dehydrogenase exist including phosphorylating and non-phosphorylating varieties and ones that transfer hydrogen to NADP and ones that transfer hydrogen to NAD.20-alpha-Hydroxysteroid Dehydrogenase: An enzymes that catalyzes the reversible reduction-oxidation reaction of 20-alpha-hydroxysteroids, such as from PROGESTERONE to 20-ALPHA-DIHYDROPROGESTERONE.Aldehyde Dehydrogenase: An enzyme that oxidizes an aldehyde in the presence of NAD+ and water to an acid and NADH. This enzyme was formerly classified as EC 1.1.1.70.Glutamate Dehydrogenase: An enzyme that catalyzes the conversion of L-glutamate and water to 2-oxoglutarate and NH3 in the presence of NAD+. (From Enzyme Nomenclature, 1992) EC 1.4.1.2.Glucosephosphate DehydrogenaseMalate Dehydrogenase: An enzyme that catalyzes the conversion of (S)-malate and NAD+ to oxaloacetate and NADH. EC 1.1.1.37.Isocitrate Dehydrogenase: An enzyme of the oxidoreductase class that catalyzes the conversion of isocitrate and NAD+ to yield 2-ketoglutarate, carbon dioxide, and NADH. It occurs in cell mitochondria. The enzyme requires Mg2+, Mn2+; it is activated by ADP, citrate, and Ca2+, and inhibited by NADH, NADPH, and ATP. The reaction is the key rate-limiting step of the citric acid (tricarboxylic) cycle. (From Dorland, 27th ed) (The NADP+ enzyme is EC 1.1.1.42.) EC 1.1.1.41.Phosphoadenosine Phosphosulfate: 3'-Phosphoadenosine-5'-phosphosulfate. Key intermediate in the formation by living cells of sulfate esters of phenols, alcohols, steroids, sulfated polysaccharides, and simple esters, such as choline sulfate. It is formed from sulfate ion and ATP in a two-step process. This compound also is an important step in the process of sulfur fixation in plants and microorganisms.Arylsulfotransferase: A sulfotransferase that catalyzes the sulfation of a phenol in the presence of 3'-phosphoadenylylsulfate as sulfate donor to yield an aryl sulfate and adenosine 3',5'-bisphosphate. A number of aromatic compounds can act as acceptors; however, organic hydroxylamines are not substrates. Sulfate conjugation by this enzyme is a major pathway for the biotransformation of phenolic and catechol drugs as well as neurotransmitters. EC 2.8.2.1.Ketosteroids: Steroid derivatives formed by oxidation of a methyl group on the side chain or a methylene group in the ring skeleton to form a ketone.Dihydrolipoamide Dehydrogenase: A flavoprotein containing oxidoreductase that catalyzes the reduction of lipoamide by NADH to yield dihydrolipoamide and NAD+. The enzyme is a component of several MULTIENZYME COMPLEXES.NADP: Nicotinamide adenine dinucleotide phosphate. A coenzyme composed of ribosylnicotinamide 5'-phosphate (NMN) coupled by pyrophosphate linkage to the 5'-phosphate adenosine 2',5'-bisphosphate. It serves as an electron carrier in a number of reactions, being alternately oxidized (NADP+) and reduced (NADPH). (Dorland, 27th ed)Carbohydrate Dehydrogenases: Reversibly catalyze the oxidation of a hydroxyl group of carbohydrates to form a keto sugar, aldehyde or lactone. Any acceptor except molecular oxygen is permitted. Includes EC 1.1.1.; EC 1.1.2.; and 1.1.99.Succinate Dehydrogenase: A flavoprotein containing oxidoreductase that catalyzes the dehydrogenation of SUCCINATE to fumarate. In most eukaryotic organisms this enzyme is a component of mitochondrial electron transport complex II.L-Iditol 2-Dehydrogenase: An alcohol oxidoreductase which catalyzes the oxidation of L-iditol to L-sorbose in the presence of NAD. It also acts on D-glucitol to form D-fructose. It also acts on other closely related sugar alcohols to form the corresponding sugar. EC 1.1.1.14Dehydroepiandrosterone: A major C19 steroid produced by the ADRENAL CORTEX. It is also produced in small quantities in the TESTIS and the OVARY. Dehydroepiandrosterone (DHEA) can be converted to TESTOSTERONE; ANDROSTENEDIONE; ESTRADIOL; and ESTRONE. Most of DHEA is sulfated (DEHYDROEPIANDROSTERONE SULFATE) before secretion.Glycerolphosphate DehydrogenaseSubstrate Specificity: A characteristic feature of enzyme activity in relation to the kind of substrate on which the enzyme or catalytic molecule reacts.Glucose 1-Dehydrogenase: A glucose dehydrogenase that catalyzes the oxidation of beta-D-glucose to form D-glucono-1,5-lactone, using NAD as well as NADP as a coenzyme.Molecular Sequence Data: Descriptions of specific amino acid, carbohydrate, or nucleotide sequences which have appeared in the published literature and/or are deposited in and maintained by databanks such as GENBANK, European Molecular Biology Laboratory (EMBL), National Biomedical Research Foundation (NBRF), or other sequence repositories.Ketoglutarate Dehydrogenase ComplexAldehyde Oxidoreductases: Oxidoreductases that are specific for ALDEHYDES.Glucose Dehydrogenases: D-Glucose:1-oxidoreductases. Catalyzes the oxidation of D-glucose to D-glucono-gamma-lactone and reduced acceptor. Any acceptor except molecular oxygen is permitted. Includes EC 1.1.1.47; EC 1.1.1.118; EC 1.1.1.119 and EC 1.1.99.10.Phosphogluconate Dehydrogenase: An enzyme of the oxidoreductase class that catalyzes the reaction 6-phospho-D-gluconate and NADP+ to yield D-ribulose 5-phosphate, carbon dioxide, and NADPH. The reaction is a step in the pentose phosphate pathway of glucose metabolism. (From Dorland, 27th ed) EC 1.1.1.43.Sugar Alcohol Dehydrogenases: Reversibly catalyzes the oxidation of a hydroxyl group of sugar alcohols to form a keto sugar, aldehyde or lactone. Any acceptor except molecular oxygen is permitted. Includes EC 1.1.1.; EC 1.1.2. and EC 1.1.99.Stereoisomerism: The phenomenon whereby compounds whose molecules have the same number and kind of atoms and the same atomic arrangement, but differ in their spatial relationships. (From McGraw-Hill Dictionary of Scientific and Technical Terms, 5th ed)Acyl-CoA Dehydrogenases: Enzymes that catalyze the first step in the beta-oxidation of FATTY ACIDS.NADH Dehydrogenase: A flavoprotein and iron sulfur-containing oxidoreductase that catalyzes the oxidation of NADH to NAD. In eukaryotes the enzyme can be found as a component of mitochondrial electron transport complex I. Under experimental conditions the enzyme can use CYTOCHROME C GROUP as the reducing cofactor. The enzyme was formerly listed as EC 1.6.2.1.IMP Dehydrogenase: An enzyme that catalyzes the dehydrogenation of inosine 5'-phosphate to xanthosine 5'-phosphate in the presence of NAD. EC 1.1.1.205.Amino Acid Sequence: The order of amino acids as they occur in a polypeptide chain. This is referred to as the primary structure of proteins. It is of fundamental importance in determining PROTEIN CONFORMATION.Lactate Dehydrogenases: Alcohol oxidoreductases with substrate specificity for LACTIC ACID.Gene Expression Regulation, Enzymologic: Any of the processes by which nuclear, cytoplasmic, or intercellular factors influence the differential control of gene action in enzyme synthesis.Isoenzymes: Structurally related forms of an enzyme. Each isoenzyme has the same mechanism and classification, but differs in its chemical, physical, or immunological characteristics.Formate Dehydrogenases: Flavoproteins that catalyze reversibly the reduction of carbon dioxide to formate. Many compounds can act as acceptors, but the only physiologically active acceptor is NAD. The enzymes are active in the fermentation of sugars and other compounds to carbon dioxide and are the key enzymes in obtaining energy when bacteria are grown on formate as the main carbon source. They have been purified from bovine blood. EC 1.2.1.2.Acyl-CoA Dehydrogenase: A flavoprotein oxidoreductase that has specificity for medium-chain fatty acids. It forms a complex with ELECTRON TRANSFERRING FLAVOPROTEINS and conveys reducing equivalents to UBIQUINONE.Xanthine Dehydrogenase: An enzyme that catalyzes the oxidation of XANTHINE in the presence of NAD+ to form URIC ACID and NADH. It acts also on a variety of other purines and aldehydes.3-Methyl-2-Oxobutanoate Dehydrogenase (Lipoamide): A ketone oxidoreductase that catalyzes the overall conversion of alpha-keto acids to ACYL-CoA and CO2. The enzyme requires THIAMINE DIPHOSPHATE as a cofactor. Defects in genes that code for subunits of the enzyme are a cause of MAPLE SYRUP URINE DISEASE. The enzyme was formerly classified as EC 1.2.4.3.Hydroxybutyrate DehydrogenaseBase Sequence: The sequence of PURINES and PYRIMIDINES in nucleic acids and polynucleotides. It is also called nucleotide sequence.Pyruvate Dehydrogenase (Lipoamide): The E1 component of the multienzyme PYRUVATE DEHYDROGENASE COMPLEX. It is composed of 2 alpha subunits (pyruvate dehydrogenase E1 alpha subunit) and 2 beta subunits (pyruvate dehydrogenase E1 beta subunit).3-Hydroxyacyl CoA Dehydrogenases: Enzymes that reversibly catalyze the oxidation of a 3-hydroxyacyl CoA to 3-ketoacyl CoA in the presence of NAD. They are key enzymes in the oxidation of fatty acids and in mitochondrial fatty acid synthesis.Ketone Oxidoreductases: Oxidoreductases that are specific for KETONES.Oxidoreductases: The class of all enzymes catalyzing oxidoreduction reactions. The substrate that is oxidized is regarded as a hydrogen donor. The systematic name is based on donor:acceptor oxidoreductase. The recommended name will be dehydrogenase, wherever this is possible; as an alternative, reductase can be used. Oxidase is only used in cases where O2 is the acceptor. (Enzyme Nomenclature, 1992, p9)Sulfates: Inorganic salts of sulfuric acid.Dihydrouracil Dehydrogenase (NADP): An oxidoreductase involved in pyrimidine base degradation. It catalyzes the catabolism of THYMINE; URACIL and the chemotherapeutic drug, 5-FLUOROURACIL.Uridine Diphosphate Glucose Dehydrogenase: An enzyme that catalyzes the oxidation of UDPglucose to UDPglucuronate in the presence of NAD+. EC 1.1.1.22.Catalysis: The facilitation of a chemical reaction by material (catalyst) that is not consumed by the reaction.Glucosephosphate Dehydrogenase Deficiency: A disease-producing enzyme deficiency subject to many variants, some of which cause a deficiency of GLUCOSE-6-PHOSPHATE DEHYDROGENASE activity in erythrocytes, leading to hemolytic anemia.

Luteinizing hormone inhibits conversion of pregnenolone to progesterone in luteal cells from rats on day 19 of pregnancy. (1/633)

We have previously reported that intrabursal ovarian administration of LH at the end of pregnancy in rats induces a decrease in luteal progesterone (P4) synthesis and an increase in P4 metabolism. However, whether this local luteolytic effect of LH is exerted directly on luteal cells or on other structures, such as follicular or stromal cells, to modify luteal function is unknown. The aim of the present study was to determine the effect of LH on isolated luteal cells obtained on Day 19 of pregnancy. Incubation of luteal cells with 1, 10, 100, or 1000 ng/ml of ovine LH (oLH) for 6 h did not modify basal P4 production. The addition to the culture medium of 22(R)-hydroxycholesterol (22R-HC, 10 microgram/ml), a membrane-permeable P4 precursor, or pregnenolone (10(-2) microM) induced a significant increase in P4 accumulation in the medium in relation to the control value. When luteal cells were preincubated for 2 h with oLH, a significant (p < 0.01) reduction in the 22R-HC- or pregnenolone-stimulated P4 accumulation was observed. Incubation of luteal cells with dibutyryl cAMP (1 mM, a cAMP analogue) plus isobutylmethylxanthine (1 mM, a phosphodiesterase inhibitor) also inhibited pregnenolone-stimulated P4 accumulation. Incubation with an inositol triphosphate synthesis inhibitor, neomycin (1 mM), or an inhibitor of intracellular Ca2+ mobilization, (8,9-N, N-diethylamino)octyl-3,4,5-trimethoxybenzoate (1 mM), did not prevent the decrease in pregnenolone-stimulated P4 secretion induced by oLH. It was concluded that the luteolytic action of LH in late pregnancy is due, at least in part, to a direct action on the luteal cells and that an increase in intracellular cAMP level might mediate this effect.  (+info)

Luteinization and proteolysis in ovarian follicles of Meishan and Large White gilts during the preovulatory period. (2/633)

This experiment was conducted to determine why follicles luteinize faster in the Meishan breed than in the Large White breed of pig. Follicles were recovered during the late follicular phase from ovaries of both breeds before and after administration of hCG given to mimic the LH surge. First, the patterns of cholesterol transporters (high and low density lipoproteins: HDL and LDL) were compared. Cholesterol transporters detected in follicular fluid consisted of HDL only. Similar amounts of Apolipoprotein A-I were found in all samples. There was no obvious breed effect on minor lipoproteins found in the HDL-rich fraction, and this pattern was altered similarly by hCG in the two breeds. The LDL-rich samples of serum from both breeds contained similar amounts of protein. Second, three steroidogenic enzymes, adrenodoxin, 17 alpha-hydroxylase-lyase (P450(17) alpha) and 3 beta-hydroxysteroid-dehydrogenase (3 beta-HSD) were detected by immunohistochemistry and quantified by image analysis on sections of the two largest follicles. Before hCG treatment, theca interna cells demonstrated immunoreactivities for adrenodoxin (strong), P450(17) alpha and 3 beta-HSD (very strong), whereas granulosa cells displayed immunoreactivities for adrenodoxin only. After hCG treatment, the localization of the enzymes was unchanged but the staining intensity of adrenodoxin on granulosa cells and 3 beta-HSD on theca cells increased (P < 0.01 and P < 0.05, respectively). Breed effects were detected for the amounts of adrenodoxin in theca cells (Meishan > Large White; P < 0.05) and of 17 alpha-hydroxylase (Large White > Meishan, P < 0.01). Breed x treatment interactions were never detected. Finally, gelatinases, plasminogen activator, plasminogen activator inhibitor, tissue inhibitors of metalloproteases (TIMP-1 and TIMP-2) were visualized by direct or reverse zymography or western blotting. Whatever the stage relative to LH administration, follicular fluid from Large White gilts contained more TIMP-1, and TIMP-2 (P < 0.02 and P < 0.01, respectively). No breed effect was detected for the amounts of gelatinases and plasminogen activator inhibitor 1. However, for these parameters, a significant breed x time interaction was obvious, as the Meishan follicles had a greater response to hCG (P < 0.01). Since proteolysis plays a key role in the bioavailability of growth factors such as insulin-like growth factor 1, fibroblast growth factor and transforming growth factor beta, which have the ability to alter gonadotrophin-induced progesterone production in pigs, the differences observed in its control in the present study may explain, at least in part, the different patterns of luteinization observed in Meishan and Large White follicles.  (+info)

Opposing changes in 3alpha-hydroxysteroid dehydrogenase oxidative and reductive activities in rat leydig cells during pubertal development. (3/633)

The enzyme 3alpha-hydroxysteroid dehydrogenase (3alpha-HSD) has an important role in androgen metabolism, catalyzing the interconversion of dihydrotestosterone (DHT) and 5alpha-androstane-3alpha,17beta-diol (3alpha-DIOL). The net direction of this interconversion will affect the amount of biologically active ligand available for androgen receptor binding. We hypothesize that in Leydig cells, differential expression of 3alpha-HSD enzymes favoring one of the two directions is a mechanism by which DHT levels are controlled. In order to characterize 3alpha-HSD in rat Leydig cells, the following properties were analyzed: rates of oxidation (3alpha-DIOL to DHT) and reduction (DHT to 3alpha-DIOL) and preference for the cofactors NADP(H) and NAD(H) (i.e., the oxidized and reduced forms of both pyridine nucleotides) in Leydig cells isolated on Days 21, 35, and 90 postpartum. Levels of 3alpha-HSD protein were measured by immunoblotting using an antibody directed against the liver type of the enzyme. Levels of 3alpha-HSD protein and rates of reduction were highest on Day 21 and lowest on Day 90. The opposite was true for the rate of 3alpha-HSD oxidation, which was barely detectable on Day 21 and highest on Day 90 (59.08 +/- 6.35 pmol/min per 10(6) cells, mean +/- SE). Therefore, the level of 3alpha-HSD protein detectable by liver enzyme was consistent with reduction but not with oxidation. There was a clear partitioning of NADP(H)-dependent activity into the cytosolic fraction of Leydig cells, whereas on Days 35 and 90, Leydig cells also contained a microsomal NAD(H)-activated 3alpha-HSD. We conclude that 1) the cytosolic 3alpha-HSD in Leydig cells on Day 21 behaves as a unidirectional NADPH-dependent reductase; 2) by Day 35, a microsomal NAD(H)-dependent enzyme activity is present and may account for predominance of 3alpha-HSD oxidation over reduction and the resultant high capacity of Leydig cells on Day 90 to synthesize DHT from 3alpha-DIOL.  (+info)

Expression of 3beta-hydroxysteroid dehydrogenase type I and type VI isoforms in the mouse testis during development. (4/633)

Six isoforms of the enzyme 3beta-hydroxysteroid dehydrogenase (3betaHSD) have been identified in the mouse, each the product of a distinct gene. Two of these isoforms (type I and type VI) are detectable in the adult testis but changes in their expression during development are unknown. In this study we have examined changes in testicular expression and localization of mRNA encoding the type I and type VI isoforms of 3betaHSD. Total 3betaHSD (type I plus type VI) mRNA was measured by reverse transcription-polymerase chain reaction and showed a peak of expression at day 5 after birth followed by a decline and then a further rise after day 10 that continued up to adulthood. When each isoform was measured individually it was clear that the type I isoform was expressed at all ages from embryonic day 13 to adulthood. In contrast, the type VI isoform was only expressed at significant levels during fetal life on embryonic day 13 and then not again until after day 10 postnatally. Expression of the type VI isoform mRNA increased markedly after day 10 so that by adulthood it was the predominant 3betaHSD isoform present in the testis. Closer examination of the timing of type VI expression showed that the isoform mRNA was first detectable at a significant level on day 11. In-situ hybridization confirmed that the type I isoform is the only one expressed in the fetal/neonatal animal and showed that expression was limited to the interstitial tissue. In the adult, both type I and type VI expression was within the interstitial tissue. The timing of 3betaHSD type VI mRNA expression suggests, strongly, that this isoform is expressed only by adult-type Leydig cells in the mouse testis and that this development starts shortly before day 11. The limited expression of the type VI isoform means that it will be a useful marker in studies of adult Leydig cell development.  (+info)

Molecular cloning and characterization of hemolymph 3-dehydroecdysone 3beta-reductase from the cotton leafworm, Spodoptera littoralis. A new member of the third superfamily of oxidoreductases. (5/633)

The primary product of the prothoracic glands of last instar larvae of Spodoptera littoralis is 3-dehydroecdysone (3DE). After secretion, 3DE is reduced to ecdysone by 3DE 3beta-reductase in the hemolymph. We have previously purified and characterized 3DE 3beta-reductase from the hemolymph of S. littoralis. In this study, cDNA clones encoding the enzyme were obtained by reverse transcription-polymerase chain reaction, employing primers based on the amino acid sequences, in conjunction with 5'- and 3'-rapid amplification of cDNA ends. Multiple polyadenylation signals and AT-rich elements were found in the 3'-untranslated region, suggesting that this region may have a role in regulation of expression of the gene. Conceptual translation and amino acid sequence analysis suggest that 3DE 3beta-reductase from S. littoralis is a new member of the third superfamily of oxidoreductases. Northern analysis shows that 3DE 3beta-reductase mRNA transcripts are widely distributed, but are differentially expressed, in some tissues. The developmental profile of the mRNA revealed that the gene encoding 3DE 3beta-reductase is only transcribed in the second half of the last larval instar and that this fluctuation in expression accounts for the change in the enzyme activity during the instar. Southern analysis indicates that the 3DE 3beta-reductase is encoded by a single gene, which probably contains at least one intron.  (+info)

An inborn error of bile acid synthesis (3beta-hydroxy-delta5-C27-steroid dehydrogenase deficiency) presenting as malabsorption leading to rickets. (6/633)

Deficiency of 3beta-hydroxy-delta5-C27-steroid dehydrogenase (3beta-HSDH), the enzyme that catalyses the second reaction in the principal pathway for the synthesis of bile acids, has been reported to present with prolonged neonatal jaundice with the biopsy features of neonatal hepatitis. It has also been shown to present between the ages of 4 and 46 months with jaundice, hepatosplenomegaly, and steatorrhoea (a clinical picture resembling progressive familial intrahepatic cholestasis). This paper reports two children with 3beta-HSDH deficiency who developed rickets during infancy and did not develop clinically evident liver disease until the age of 3 years. Bile acid replacement resulted in considerable clinical and biochemical improvement. The importance of thorough investigation of fat soluble vitamin deficiencies in infancy is emphasised.  (+info)

Dynamics of periovulatory steroidogenesis in the rhesus monkey follicle after ovarian stimulation. (7/633)

The temporal relationships and regulation of events in the primate follicle during the periovulatory interval are poorly understood. This study was designed to elucidate the dynamics of steroid synthesis in the macaque follicle during ovarian stimulation cycles in which serum/follicular fluid aspirates were collected at precise intervals before (0 h) and after (up to 36 h) administration of the ovulatory human chorionic gonadotrophin (HCG) bolus. Serum concentrations of progesterone increased (P < 0.05) within 30 min, and follicular fluid progesterone concentrations were elevated 180-fold within 12 h, of HCG injection, and remained elevated until the time of ovulation. In contrast, 17beta-oestradiol concentrations increased initially, but then declined (P < 0.05) by 36 h post-HCG. Acute incubation of granulosa cells with and without steroidogenic substrates demonstrated that: (i) 3beta-hydroxysteroid dehydrogenase and aromatase activities were present in equivalent amounts before and after HCG; whereas (ii) P450 side-chain cleavage activity increased (P < 0.05) within 12 h of HCG; and (iii) exogenous low-density lipoprotein and cholesterol were not utilized for steroidogenesis. This model should be useful for further studies on ovulation and luteinization in primates, and enable elucidation of the local actions of progesterone and other steroids at specific time points during the periovulatory interval.  (+info)

Paracrine glucocorticoid activity produced by mouse thymic epithelial cells. (8/633)

Previous data have suggested that glucocorticoids (GCs) are involved in the differentiation of thymocytes into mature T cells. In this report we demonstrate that the mouse thymic epithelial cells (TEC) express the cytochrome P450 hydroxylases Cyp11A1, Cyp21, and Cyp11B1. These enzymes, in combination with 3beta-hydroxysteroid dehydrogenase (3betaHSD), convert cholesterol into corticosterone, the major GC in rodents. In addition, when TEC were cocultured with 'reporter cells' containing the glucocorticoid receptor (GR) and a GR-dependent reporter gene, a specific induction of reporter gene activity was observed. Induction of reporter gene activity was blocked when the TEC and reporter cells were incubated in the presence of the Cyp11B1 inhibitor metyrapone or the 3betaHSD inhibitor trilostane, as well as by the GR antagonist RU486. Coculturing of TEC with thymocytes induced apoptosis in the latter, which was partially blocked by the enzyme inhibitors and RU486. We conclude that TEC secrete a GC hormone activity and suggest a paracrine role for this in thymocyte development.  (+info)

Mouse polyclonal antibody raised against a partial recombinant NSDHL. NSDHL (NP_057006, 1 a.a. ~ 110 a.a) partial recombinant protein with GST tag. (H00050814-A01) - Products - Abnova
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TY - JOUR. T1 - The orphan nuclear receptor, liver receptor homolog-1, regulates cholesterol side-chain cleavage cytochrome P450 enzyme in human granulosa cells. AU - Kim, Joung W.. AU - Havelock, Jon C.. AU - Carr, Bruce R.. AU - Attia, George R.. PY - 2005/3/1. Y1 - 2005/3/1. N2 - After ovulation, there is a shift in ovarian steroidogenesis from an estrogen-producing ovarian follicle to a progesterone-producing corpus luteum. The first step in human ovarian steroidogenesis is catalyzed by cholesterol side-chain cleavage cytochrome P450 (CYP11A1) enzyme. Steroidogenic factor-1 is an orphan nuclear receptor that regulates several steroidogenic enzymes, including CYP11A1. Liver receptor homolog-1 (LRH-1) is another orphan nuclear receptor that is expressed in the human ovary. After ovulation there is a down-regulation in steroidogenic factor-1, which is associated with an up-regulation of LRH-1 expression. These changes coincide with increased level of CYP11A1 expression in human corpus luteum. ...
K00498 CYP11A; cholesterol monooxygenase (side-chain-cleaving) [EC:1.14.15.6] K00512 CYP17A; steroid 17alpha-monooxygenase / 17alpha-hydroxyprogesterone deacetylase [EC:1.14.14.19 1.14.14.32] K01131 STS; steryl-sulfatase [EC:3.1.6.2] K01015 SULT2B1; alcohol sulfotransferase [EC:2.8.2.2] K00513 CYP21A; steroid 21-monooxygenase [EC:1.14.14.16] K00070 HSD3B; 3beta-hydroxy-Delta5-steroid dehydrogenase / steroid Delta-isomerase [EC:1.1.1.145 5.3.3.1] K00070 HSD3B; 3beta-hydroxy-Delta5-steroid dehydrogenase / steroid Delta-isomerase [EC:1.1.1.145 5.3.3.1] K00070 HSD3B; 3beta-hydroxy-Delta5-steroid dehydrogenase / steroid Delta-isomerase [EC:1.1.1.145 5.3.3.1] K00070 HSD3B; 3beta-hydroxy-Delta5-steroid dehydrogenase / steroid Delta-isomerase [EC:1.1.1.145 5.3.3.1] K00070 HSD3B; 3beta-hydroxy-Delta5-steroid dehydrogenase / steroid Delta-isomerase [EC:1.1.1.145 5.3.3.1] K00070 HSD3B; 3beta-hydroxy-Delta5-steroid dehydrogenase / steroid Delta-isomerase [EC:1.1.1.145 5.3.3.1] K12343 SRD5A1; ...
20α-Hydroxysteroid dehydrogenase (20α-HSD), which metabolizes progesterone to an inactive steroid in the corpus luteum of mice and rats but not of humans, is thought to play a crucial role in shortening the oestrous cycles in these rodent species. We determined the nucleotide sequence of the 5′-flanking region of the mouse 20α-HSD gene, and examined its promoter activity using a rat luteinized granulosa cell culture. A reporter assay, using reporter constructs of various lengths of the 5′-flanking region, revealed that the region between −83 and 60 bp upstream of the transcription start site was essential for transcriptional activity. Furthermore, mutational analysis demonstrated that a putative Sp1 site in this region was critical to the expression of the reporter gene. Electrophoretic mobility-shift assays showed that the interaction of proteins in a nuclear extract from rat luteinized granulosa cells with this region was inhibited by a competitor having the wild-type Sp1 sequence in ...
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1I5R: A concerted, rational design of type 1 17beta-hydroxysteroid dehydrogenase inhibitors: estradiol-adenosine hybrids with high affinity
17β-Hydroxysteroid dehydrogenases (HSD17Bs) comprise a large family of 15 members that are mainly involved in sex hormone metabolism. Some HSD17Bs enzymes also play key roles in cholesterol and fatty acid metabolism. Recent study showed that hydroxysteroid 17β-dehydrogenase 13 (HSD17B13), an enzyme …
Trilostane is the chemical name for a medication that effectively treats Canine Cushings Disease. Worldwide, the only licensed veterinary version of trilostane is manufactured in the U.K. by the Dechra Group under the brand name of Vetoryl. Vetoryl is marketed in four dosage strengths: 10 mg., 30 mg., 60 mg., and 120 mg. capsules. Vetoryl is commonly used in the U.K. and Europe, and it is becoming more widely prescribed in the U.S. subsequent to FDA approval beginning in 2009. All dosage
The enzyme 20α-hydroxysteroid dehydrogenase (20α-HSD) catalyzes the conversion of progesterone to its inactive form, 20α-hydroxyprogesterone. This enzyme has been shown to play a critical role in the regulation of luteal function in experimental animals. In this study, we cloned and expressed the gene encoding elk deer 20α-HSD from reproductive placental ...
The research in the Schlinger lab focuses on two questions: 1) How are steroids made available in active forms to distinct neural circuits at appropriate periods of the animals life? 2) How have some neural circuits, but not others, become sensitive to control by steroidal signalling molecules? Experimental Approaches: We study birds in the lab and in the field to explore these questions, examining species that have evolved unique behavioral strategies to optimize their reproductive potential. Techniques regularly used by members of the laboratory include: biochemical assays of steroidogenic enzyme activity, steroidogenic enzyme mRNA expression via Northern blots, rtPCR/Southern blots, in situ hybridization, protein expression via immunocytochemistry, Western blots, neuroanatomical measures via light and fluorescence microscopy and image analysis, and steroid-autoradiography. Please click on the links to learn more about our lab! ...
Abstract Interference with the pregnancy-maintaining influence of progesterone is the basis of most methods for termination of unwanted pregnancy in dogs. The currently available methods are based on induction of luteolysis or blocking of the progesterone receptor. Inhibition of progesterone synthesis using a competitive inhibitor of 3 -hydroxysteroid dehydrogenase (3 ... read more -HSD) could be another strategy to terminate unwanted pregnancies. In this study we investigated the effects of the 3 -HSD inhibitor trilostane on corpus luteum function in non-pregnant bitches. Trilostane was administered orally for seven consecutive days in either the pituitary-independent part of the luteal phase (PIP, start of treatment on D11 after ovulation, n 6) or the pituitary-dependent part (PDP, start of treatment on D31 after ovulation, n 6), in an oral dose of about 4.5 mg/kg bw, twice daily. Results were compared with those obtained in control bitches (n 6). ACTH stimulation tests were performed to ...
Musto, N; Hafiez, A A.; and Bartke, A, "Prolactin increases 17beta-hydroxysteroid dehydrogenase activity in the testis." (1972). Subject Strain Bibliography 1972. 2710 ...
The primary source of oestrogen in premenopausal women is the ovary but, after menopause, oestrogen biosynthesis in peripheral tissue is the exclusive site of formation. An enzyme group that affects the availability of active oestrogens is the 17β-hydroxysteroid dehydrogenase (17HSD) family. In breast cancer, 17HSD type 1 and type 2 have been mostly investigated and seem to be the principal 17HSD enzymes involved thus far. The question whether 17HSD type 1 or type 2 is of greatest importance in breast tumour development is still not clear. The aim of this study was to investigate how the loss of 17HSD type 2 expression, using siRNA in the non-tumour breast epithelial cells HMEC (human mammal epithelial cells) and MCF10A, and gain of 17HSD type 2 expression, using transient transfection in the breast cancer derived cell lines MCF7 and T47D, affect oestradiol conversion and proliferation rate measured as S-phase fraction. We further investigated how this was related to the endogenous expression ...
3-beta-HSD is a bifunctional enzyme, that catalyzes the oxidative conversion of Delta(5)-ene-3-beta-hydroxy steroid, and the oxidative conversion of ketosteroids. The 3-beta-HSD enzymatic system plays a crucial role in the biosynthesis of all classes of hormonal steroids.
The biosynthesis of steroid hormones in the gonads and adrenal glands requires the activities of the enzyme 3 beta-hydroxysteroid dehydrogenase/isomerase (3 beta HSD) which catalyzes the NAD(+)-dependent dehydrogenation and subsequent delta 5--|delta 4 isomerization of delta 5-3 beta-hydroxysteroids to delta 4-3-ketosteroids. The mouse expresses four isoforms of 3 beta HSD. 3 beta HSD I is expressed in gonads and adrenal glands and appears to be the major steroidogenic form, 3 beta HSDs II and III are expressed in both liver and kidneys, and 3 beta HSD IV has been detected only in kidneys. To determine the genetic relationship between the 3 beta HSD isoforms, we have mapped the chromosomal locations of the four genes by linkage analysis using gene-specific probes derived from the 3 untranslated regions of 3 beta HSD cDNA clones. The four 3 beta HSD structural genes (Hsd3b) are closely linked within a segment of chromosome 3 that is conserved on human chromosome 1. The order of markers on
Accepted name: 17β-estradiol 17-dehydrogenase. Reaction: 17β-estradiol + NAD(P)+ = estrone + NAD(P)H + H+. Other name(s): 20α-hydroxysteroid dehydrogenase; 17β,20α-hydroxysteroid dehydrogenase; 17β-estradiol dehydrogenase; estradiol dehydrogenase; estrogen 17-oxidoreductase; 17β-HSD; HSD17B7. Systematic name: 17β-estradiol:NAD(P)+ 17-oxidoreductase. Comments: The enzyme oxidizes or reduces the hydroxy/keto group on C17 of estrogens and androgens in mammals and regulates the biological potency of these steroids. The mammalian enzyme is bifunctional and also catalyses EC 1.1.1.270, 3β-hydroxysteroid 3-dehydrogenase [3]. The enzyme also acts on (S)-20-hydroxypregn-4-en-3-one and related compounds, oxidizing the (S)-20-group, but unlike EC 1.1.1.149, 20α-hydroxysteroid dehydrogenase, it is Si-specific with respect to NAD(P)+.. Links to other databases: BRENDA, EXPASY, GTD, KEGG, Metacyc, PDB, CAS registry number: 9028-61-9. References:. 1. Kautsky, M.P. and Hagerman, D.D. 17β-Estradiol ...
Accepted name: 17β-estradiol 17-dehydrogenase. Reaction: 17β-estradiol + NAD(P)+ = estrone + NAD(P)H + H+. Other name(s): 20α-hydroxysteroid dehydrogenase; 17β,20α-hydroxysteroid dehydrogenase; 17β-estradiol dehydrogenase; estradiol dehydrogenase; estrogen 17-oxidoreductase; 17β-HSD; HSD17B7. Systematic name: 17β-estradiol:NAD(P)+ 17-oxidoreductase. Comments: The enzyme oxidizes or reduces the hydroxy/keto group on C17 of estrogens and androgens in mammals and regulates the biological potency of these steroids. The mammalian enzyme is bifunctional and also catalyses EC 1.1.1.270, 3β-hydroxysteroid 3-dehydrogenase [3]. The enzyme also acts on (S)-20-hydroxypregn-4-en-3-one and related compounds, oxidizing the (S)-20-group, but unlike EC 1.1.1.149, 20α-hydroxysteroid dehydrogenase, it is Si-specific with respect to NAD(P)+.. Links to other databases: BRENDA, EXPASY, GTD, KEGG, Metacyc, PDB, CAS registry number: 9028-61-9. References:. 1. Kautsky, M.P. and Hagerman, D.D. 17β-Estradiol ...
Aldo-keto reductase family 1 member C1 also known as 20α-hydroxysteroid dehydrogenase, 3α-hydroxysteroid dehydrogenase, and dihydrodiol dehydrogenase 1/2 is an enzyme that in humans is encoded by the AKR1C1 gene.[1][2] This gene encodes a member of the aldo/keto reductase superfamily, which consists of more than 40 known enzymes and proteins. These enzymes catalyze the conversion of aldehydes and ketones to their corresponding alcohols by utilizing NADH and/or NADPH as cofactors. The enzymes display overlapping but distinct substrate specificity. This enzyme catalyzes the reduction of progesterone to the inactive form 20-alpha-hydroxy-progesterone. This gene shares high sequence identity with three other gene members, and is clustered with those three genes at chromosome 10p15-p14.[2] ...
USP Grape Seed Oil. If you prefer, you also could replace grape seed oil into ethyl oleate or MCT.. Drostanolone Enanthate Introduction and Usage:. Masteron is a modified form of Dihydrotestosterone, with a methyl group at the 2nd carbon (carbon alpha) atom. This modification is responsible for the anabolic strength increase. This methyl group makes it harder for the enzyme 3-hydroxysteroid dehydrogenase to metabolize Masteron. This enzyme is abundantly present in muscle tissue, and is responsible for degrading any DHT into two inactive metabolites: 3-Alpha Androstanediol and 3-Beta Androstanediol. Because of this enzyme DHT is not anabolic in muscle tissue at all. It is believed that if the enzyme 3-hydroxysteroid dehydrogenase was neutralized, DHT would actually be a very powerful anabolic steroid. Drostanolones methyl group addition makes it imune to this enzyme.. Drostanolone is injected into the body as an ester (bonded to either Propionate or Enanthate). Enzymes cleave off the ester from ...
Androgens and estrogens increase the number of cell division and the opportunity for random genetic errors and are thus involved in carcinogenesis of hormone related cancers. [...]
Homo sapiens aldo-keto reductase family 1, member C1 (dihydrodiol dehydrogenase 1; 20-alpha (3-alpha)-hydroxysteroid dehydrogenase) (AKR1C1), mRNA. (H00001645-R01) - Products - Abnova
aldo-keto reductase family 1, member C2 (dihydrodiol dehydrogenase 2; bile acid binding protein; 3-alpha hydroxysteroid dehydrogenase, type III ...
To this day, a significant proportion of the human genome remains devoid of functional characterization. In this study, we present evidence that the previously functionally uncharacterized product of the human DHRS10 gene is endowed with 17beta-HSD (17beta-hydroxysteroid dehydrogenase) activity. 17beta-HSD enzymes are primarily involved in the metabolism of steroids at the C-17 position and also of other substrates such as fatty acids, prostaglandins and xenobiotics. In vitro, DHRS10 converts NAD+ into NADH in the presence of oestradiol, testosterone and 5-androstene-3beta,17beta-diol. Furthermore, the product of oestradiol oxidation, oestrone, was identified in intact cells transfected with a construct plasmid encoding the DHRS10 protein. In situ fluorescence hybridization studies have revealed the cytoplasmic localization of DHRS10. Along with tissue expression data, this suggests a role for DHRS10 in the local inactivation of steroids in the central nervous system and placenta. The crystal structure
CP001022.PE374 Location/Qualifiers FT CDS_pept 400861..401859 FT /codon_start=1 FT /transl_table=11 FT /locus_tag="Exig_0378" FT /product="UDP-glucose 4-epimerase" FT /note="TIGRFAM: UDP-glucose 4-epimerase; PFAM: FT NAD-dependent epimerase/dehydratase; short-chain FT dehydrogenase/reductase SDR; 3-beta hydroxysteroid FT dehydrogenase/isomerase; polysaccharide biosynthesis FT protein CapD; dTDP-4-dehydrorhamnose reductase; Male FT sterility domain; KEGG: bld:BLi04283 hypothetical protein" FT /db_xref="EnsemblGenomes-Gn:Exig_0378" FT /db_xref="EnsemblGenomes-Tr:ACB59862" FT /db_xref="GOA:B1YIH9" FT /db_xref="InterPro:IPR001509" FT /db_xref="InterPro:IPR005886" FT /db_xref="InterPro:IPR036291" FT /db_xref="UniProtKB/TrEMBL:B1YIH9" FT /protein_id="ACB59862.1" FT /translation="MAVLVVGGAGYIGSHAVYQLVDAGQDVVVIDHLKSGHREAVHPKA FT RFYEGDIRDRAFLDTVFEKETIDQVVHFAAFSLVGESMEHPLAYFDNNVYGTQVLLEAM FT MAHDVKQIVFSSTAATYGEQEQMPILETATTNPTNAYGETKLMMEKMMRWCETAYGLNY FT ...
Life Sci. 2001 Jan 5;68(7):751-61. Links Chalcones are potent inhibitors of aromatase and 17beta-hydroxysteroid dehydrogenase activities.Le Bail JC,
Shop Inactive hydroxysteroid dehydrogenase-like protein ELISA Kit, Recombinant Protein and Inactive hydroxysteroid dehydrogenase-like protein Antibody at MyBioSource. Custom ELISA Kit, Recombinant Protein and Antibody are available.
Aged, Aromatase, Breast Neoplasms, England, Estradiol, Female, Genotype, Health Surveys, Humans, Hydroxysteroid Dehydrogenases, Middle Aged, Polymorphism, Genetic, Postmenopause, Risk Factors, Steroid 17-alpha-Hydroxylase. ...
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The IUPHAR/BPS Guide to Pharmacology. trilostane ligand page. Quantitative data and detailed annnotation of the targets of licensed and experimental drugs.
Kit Component:- KN307977G1, Hsd3b2 gRNA vector 1 in pCas-Guide vector- KN307977G2, Hsd3b2 gRNA vector 2 in pCas-Guide vector- KN307977D, donor vector…
Hydroxysteroid (17-beta) Dehydrogenase 4兔多克隆抗体(ab97971)可与人样本反应并经WB实验严格验证。所有产品均提供质保服务,中国75%以上现货。
Looking for information on 3 beta hydroxysteroid dehydrogenase deficiency? Medigest has all you need to know about 3 beta hydroxysteroid dehydrogenase deficiency - Symptoms and Signs, Causes, Treatments and definition
Girls with idiopathic premature adrenarche, characterized by the early appearance of pubic hair and adrenal hyperandrogenism, may be at an increased risk for polycystic ovarian syndrome and its associated complications. Alterations of peripheral metabolism of adrenal steroids, specifically increased 5 alpha-reductase and 11 beta-hydroxysteroid dehydrogenase activities, have been documented in patients with polycystic ovarian syndrome and proposed as an underlying mechanism for the adrenal hyperandrogenism in this syndrome. We sought to investigate whether alterations in 5 alpha-reductase and 11 beta-hydroxysteroid dehydrogenase activities are present in girls with premature adrenarche, suggesting a possible role in the pathogenesis of the hyperandrogenism of this condition. We studied C19 and C21 urinary steroid metabolites, 5 alpha/5 beta and 11 oxo/11 hydroxy metabolite pairs as well as the ratios of the total 5 alpha/total 5 beta and total 11 oxo/total 11 hydroxy metabolites in 24-h urine samples
Trilostane. Currently the most common method for treating pituitary-dependent hyperadrenocorticism (PDH) in Europe is oral administration of trilostane on a daily basis. Trilostane is a synthetic, orally active steroid analogue that competitively inhibits 3β hydroxysteroid dehydrogenase and hence synthesis of several steroids, including cortisol and aldosterone. This competitive inhibition is reversible and seems to be dose-related. There is also increasing evidence to suggest that trilostane may modify peripheral conversion of cortisol to cortisone and cause some degree of adrenocortical destruction in dogs with PDH.. In dogs peak trilostane concentrations are seen within 1.5 hours of dosing and decrease to baseline values in about 18 hours. Trilostane is variably absorbed after oral administration, at least partly due to its poor water solubility. Absorption may be enhanced by administering the drug with food although this phenomenon has not been investigated in dogs with ...
Testosterone is metabolized in various tissues by 5α-reductase into DHT, which is 3- to 10-fold more potent as an AR agonist, and by aromatase into estradiol, which is an estrogen and lacks significant AR affinity.[1] In addition, DHT is metabolized by 3α-hydroxysteroid dehydrogenase (3α-HSD) and 3β-hydroxysteroid dehydrogenase (3β-HSD) into 3α-androstanediol and 3β-androstanediol, respectively, which are metabolites with little or no AR affinity.[1] 5α-Reductase is widely distributed throughout the body, and is concentrated to various extents in skin (particularly the scalp, beard-area of the face, pubic area, and genital area (penis and scrotum)), prostate, seminal vesicles, liver, and the brain.[1] In contrast, expression of 5α-reductase in skeletal muscle is undetectable.[1] Aromatase is highly expressed in adipose tissue and the brain, and is also expressed significantly in skeletal muscle.[1] 3α-HSD is also highly expressed in skeletal muscle.[56]. Natural AAS like testosterone ...
AKR1C3 - AKR1C3 (untagged)-Human aldo-keto reductase family 1, member C3 (3-alpha hydroxysteroid dehydrogenase, type II) (AKR1C3) available for purchase from OriGene - Your Gene Company.
trans-1,2-dihydrobenzene-1,2-diol dehydrogenase: rat liver cytosol enzyme also catalyzes 3alpha-hydroxysteroid dehydrogenase activity (EC 1.1.1.50); GenBank AH009074 (rat); RefSeq NM_001818 (human)
1. Actions of CRH on the Fetal Adrenal Gland As discussed in Chapter 3 (see Fetal Adrenal Glands), the human fetal adrenal glands are morphologically, functionally, and physiologically remarkable organs. At term, the fetal adrenal glands weigh the same as those in the adult and are similar in size to the adjacent fetal kidney. The…
Macdonald, I.A., Mahony, D.E., Jellett, J.F. and Meier, C.E. (1977). "NAD-dependent 3α- and 12α-hydroxysteroid dehydrogenase activities from Eubacterium lentum ATCC no. 25559". Biochim. Biophys. Acta 489: 466-476. PMID 201289. ...
1J96: Structure of the human 3alpha-hydroxysteroid dehydrogenase type 3 in complex with testosterone and NADP at 1.25-A resolution.
Achim Recktenwald, PhD (achim at ibex.ca) wrote: : Robert S. Strauss wrote: : , : , Maxy Mariasegaram ,mariaseg at HERCULES.CS.UREGINA.CA, wrote: : , : , ,Hello everyone, : , : , ,I have to write a paper on the above enzyme as part of the course : , ,requirements for a fourth year biochemistry class. : , : , ,I would appreciate any leads to literature that cover the structure, : , ,function, kinetics and recent development on 3-beta HSD, preferably some : , ,review articles. Failing which, what would be a good way to start this : , ,search? I tried looking up the Bio Abstracts, but that didnt help much. : , : , ,I look forward to hearing from people out there, and thank you very much : , ,for reading this message. : , : , ,cheers, : , ,Max Youll find a lot of information if you search medline with the words : short-chain dehydrogenases. In 1995 Jornvall et al. published a review in Biochemistry, it is pretty informative, although incomplete. Lluis ...
The enzyme 11β-hydroxysteroid dehydrogenase type 2 (11β-HSD2) is selectively expressed in aldosterone target tissues, conferring aldosterone selectivity for the mineralocorticoid receptor. A diminished activity causes salt-sensitive hypertension. The mechanism of the variable and distinct 11β-hydroxysteroid dehydrogenase type 2 gene (HSD11B2) expression in the cortical collecting duct is poorly understood. Here, we analyzed for the first time whether the 11β-HSD2 expression is modulated by microRNAs (miRNAs). In silico analysis revealed 53 and 27 miRNAs with potential binding sites on human or rat HSD11B2 3′-untranslated region. A reporter assay demonstrated 3′-untranslated region-dependent regulation of human and rodent HSD11B2. miRNAs were profiled from cortical collecting ducts and proximal convoluted tubules. Bioinformatic analyses showed a distinct clustering for cortical collecting ducts and proximal convoluted tubules with 53 of 375 miRNAs, where 13 were predicted to bind to the ...
Journal Article: On-column ligand exchange for structure-based drug design: a case study with human 11[beta]-hydroxysteroid dehydrogenase type 1 ...
11ß-hydroxysteroid dehydrogenase type1 (11β-HSD1) converts inactive glucocorticoids to active glucocorticoids which, in excess, leads to development of the various risk factors of the metabolic syndrome. Recent studies clearly suggest that both increased expression and activity of 11β-HSD1 in metabolically active tissues such as liver, muscle and adipose are implicated in tissue specific dysregulation which collectively contribute to the whole body pathology seen in metabolic syndrome. In the present study we have evaluated CNX-010-49, a highly potent, selective and pan tissue acting 11β-HSD1 inhibitor, for its potential to modulate multiple risk factors of the metabolic syndrome. Male C57B6/J mice on high fat diet (DIO mice) were orally dosed with CNX-010-49 (30 mg/kg twice daily; n = 8) or vehicle for 10 weeks. Fasting glucose, triglycerides, glycerol, free fatty acids, body weight and feed intake were measured at selected time points. At the end of the treatment an OGTT and subsequently organ
Status of 17β-hydroxysteroid dehydrogenase type 2 (17βHSD2) immunoreactivity was significantly higher in invasive lobular carcinoma (ILC) than in invasive duc
There are increasing data on the central role of miRNAs in the development of various diseases, including some kidney and cardiovascular entities.27,32,33 Whether miRNAs and the 3′-UTR of specific players in the field of renal or blood pressure physiology are relevant is yet to be addressed specifically. The 11β-HSD2 is an essential enzyme for blood pressure control.3 Therefore, the mechanisms accounting for its regulation are a prerequisite for understanding blood pressure in health and disease states. Here, we present evidence that HSD11B2 mRNA fulfills the prerequisites to be modulated by miRNAs. Because a multitude of miRNAs directly or indirectly affect the expression of a protein, special emphasis was given to the miRNA expression profile in the CCD, the main site of 11β-HSD2 action.. To the best of our knowledge, the relationship between miRNA and 11β-HSD2 was reported previously only once.34 Shang et al34 starved a human placental cell line (BeWo) from amino acids and observed a ...
The present study indicates that de novo biosynthesis of progestogens and androgens from cholesterol is unlikely in human adipose tissue, because the mRNAs of key steroidogenic enzymes, such as cytochromes P450scc and P45c17, and of proteins specifically expressed in steroidogenic cells, such as StAR and SF-1, could not be demonstrated in any of the samples. The failure to amplify cytochrome P450c17 cDNA, even with two other sets of primers (data not shown), is at variance with the report by Puche and co-workers (2002), but can be explained by the fact that they used not only RT-PCR, but also Southern blotting analysis to intensify the signal. The level of expression must be minimal anyway.. Our data support an intracrine role of adipose tissue as a terminal activator of circulating inactive androgen precursors into potent sex steroids. The detection of P450arom mRNA confirms previous findings about the occurrence of aromatizing activity for estrogen synthesis in adipose tissue, as reviewed by ...
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Hydroxysteroid Dehydrogenase (3.BETA.-HSD), 17.ALPHA.-Hydroxylase and 17, 20 Lyase by Progestins and Danazol". Endocrinologia ... 141-. ISBN 978-3-319-14385-9. CS1 maint: Multiple names: authors list (link) Bromham, D. R.; Booker, M. W.; Rose, Gillian; ... ISBN 978-3-88763-075-1. Dr. Ian Morton; I.K. Morton; Judith M. Hall (31 October 1999). Concise Dictionary of Pharmacological ... 36 (3): 387-394. doi:10.1507/endocrj1954.36.387. ISSN 0013-7219. Tamaya T, Fujimoto J, Watanabe Y, Arahori K, Okada H (1986). " ...
17β-Hydroxysteroid dehydrogenase 3 (17β-HSD3) is an enzyme that in humans is encoded by the HSD17B3 gene and is involved in ... "Entrez Gene: HSD17B3 hydroxysteroid (17-beta) dehydrogenase 3". Ademola Akesode F, Meyer WJ, Migeon CJ (December 1977). "Male ... 17β-Hydroxysteroid dehydrogenase GRCh38: Ensembl release 89: ENSG00000130948 - Ensembl, May 2017 GRCm38: Ensembl release 89: ... Rösler A, Silverstein S, Abeliovich D (May 1996). "A (R80Q) mutation in 17 beta-hydroxysteroid dehydrogenase type 3 gene among ...
Rosler, A (August 2006). "17 beta-hydroxysteroid dehydrogenase 3 deficiency in the Mediterranean population". Pediatric ... glucose-6-phosphate dehydrogenase deficiency, and fragile X syndrome (FXS), which is an inherited genetic condition with ... glucose-6-phosphate dehydrogenase deficiency, alpha-thalassemia, molecular characterization, recessive osteoperosis, ... 16 (3): 374-86. doi:10.1038/sj.ejhg.5201934. PMID 17928816. Abu-Amero, KK; Hellani, A; González, AM; Larruga, JM; Cabrera, VM; ...
"The biological activity of 3alpha-hydroxysteroid oxido-reductase in the spinal cord regulates thermal and mechanical pain ... Less than 3% of a dose is excreted in unconjugated form. With intramuscular administration, the high levels of MPA in the blood ... MPA is described as extremely potent in its inhibition of rat 3α-HSD, with an IC50 of 0.2 μM and a Ki (in rat testicular ... ISBN 978-3-527-60749-5. Archived from the original on 2017-11-05. "WHO Model List of Essential Medicines (19th List)" (PDF). ...
Couture JF, Legrand P, Cantin L, Luu-The V, Labrie F, Breton R (Aug 2003). "Human 20alpha-hydroxysteroid dehydrogenase: ... Zhang Y, Dufort I, Rheault P, Luu-The V (Oct 2000). "Characterization of a human 20alpha-hydroxysteroid dehydrogenase". Journal ... Aldo-keto reductase family 1 member C1 also known as 20α-hydroxysteroid dehydrogenase, 3α-hydroxysteroid dehydrogenase, and ... hydroxysteroid dehydrogenase)". Human AKR1C1 genome location and AKR1C1 gene details page in the UCSC Genome Browser. Human C9 ...
Aldo-keto reductase family 1 member C3 (AKR1C3), also known as 17β-hydroxysteroid dehydrogenase type 5 (17β-HSD5, HSD17B5) is a ... Rheault P, Dufort I, Soucy P, Luu-The V (1999). "Assignment of HSD17B5 encoding type 5 17 beta-hydroxysteroid dehydrogenase to ... "Human 3alpha-hydroxysteroid dehydrogenase isoforms (AKR1C1-AKR1C4) of the aldo-keto reductase superfamily: functional ... "Close kinship of human 20alpha-hydroxysteroid dehydrogenase gene with three aldo-keto reductase genes". Genes to Cells. 5 (2): ...
Subsequently, 20α-hydroxysteroid dehydrogenase and 20β-hydroxysteroid dehydrogenase reduce these metabolites to form the ... Progesterone is highly susceptible to enzymatic reduction via reductases and hydroxysteroid dehydrogenases due to its double ... First, the 3β-hydroxyl group is oxidized to a keto group and second, the double bond is moved to C4, from C5 through a keto/ ... 27 (3): 229-39. doi:10.1055/s-0029-1216276. PMC 2675922 . PMID 19401954. Li Z, Wang B, Kan Z, Zhang B, Yang Z, Chen J, Wang D, ...
However, the initial 5α-reduced metabolite of D4A, 3-keto-5α-abiraterone, is an agonist of the AR, and has been found to ... D4A is specifically an inhibitor of CYP17A1 (17α-hydroxylase/17,20-lyase), 3β-HSD, and 5α-reductase. In addition, it has also ... Δ4-Abiraterone (D4A; code name CB-7627), also known as 17-(3-pyridyl)androsta-4,16-dien-3-one, is a steroidogenesis inhibitor ... 3β-HSD). It is said to be a more potent inhibitor of steroidogenesis than abiraterone, and is partially responsible for the ...
... or 17-beta-hydroxysteroid dehydrogenase deficiency (17beta-HSD-3). A relative handful of male to female changes have been ... "17β-Hydroxysteroid dehydrogenase-3 deficiency: A rare endocrine cause of male-to-female sex reversal". Gynecological ... XY Persons with 5α-Reductase-2 Deficiency and 17β-Hydroxysteroid Dehydrogenase-3 Deficiency". Archives of Sexual Behavior. 34 ( ...
1999). "Localization of type 5 17beta-hydroxysteroid dehydrogenase, 3beta-hydroxysteroid dehydrogenase, and androgen receptor ... "Immunoelectron microscopic localization of 3beta-hydroxysteroid dehydrogenase and type 5 17beta-hydroxysteroid dehydrogenase in ... HSD3B1 is a human gene that encodes for a 3beta-hydroxysteroid dehydrogenase/delta(5)-delta(4)isomerase type I or hydroxy-delta ... Bonenfant M, Provost PR, Drolet R, Tremblay Y (2000). "Localization of type 1 17beta-hydroxysteroid dehydrogenase mRNA and ...
... alpha-hydroxysteroid dehydrogenase for neurosteroids and its inhibition by benzodiazepines" (pdf). Biological & Pharmaceutical ... 37 (1-3): 116-32. doi:10.1016/s0165-0173(01)00112-6. PMID 11744080. Su TP, London ED, Jaffe JH (1988). "Steroid binding at ... 186 (3): 362-72. doi:10.1007/s00213-005-0213-2. PMID 16432684. Dhir A, Rogawski MA (April 2012). "Role of neurosteroids in the ... 4,16-Androstadien-3β-ol (PH94B, Aloradine) is a synthetic pheromone, or pherine, neurosteroid which is under investigation for ...
9 (3): 151-7. doi:10.1007/s00737-005-0111-y. PMID 16292466. Hansen RA, Gaynes BN, Gartlehner G, Moore CG, Tiwari R, Lohr KN ( ... 25 (3): 193-200. doi:10.1002/hup.1106. PMID 20373470. Meyer JH, Wilson AA, Sagrati S, Hussey D, Carella A, Potter WZ, Ginovart ... Suppl 3: 22-34. PMID 11229450. Croft H, Settle E, Houser T, Batey SR, Donahue RM, Ascher JA (1999). "A placebo-controlled ... 3: 113-148. doi:10.1016/S1067-5698(06)80005-2. ISBN 978-1-55938-798-9. Sarges R, Tretter JR, Tenen SS, Weissman A (1973). "5,8- ...
... is a human gene that encodes for 3beta-hydroxysteroid dehydrogenase/delta(5)-delta(4)isomerase type II or hydroxy-delta- ... 5-steroid dehydrogenase, 3 beta- and steroid delta-isomerase 2. It is expressed principally in steroidogenic tissues and is ... HSD3B2 Hydroxy-delta-5-steroid dehydrogenase, 3 beta- and steroid delta-isomerase 2". Pelletier G, Dupont E, Simard J, Luu-The ... 78 (3): 561-7. doi:10.1210/jc.78.3.561. PMID 8126127. Mendonça BB, Russell AJ, Vasconcelos-Leite M, et al. (1994). "Mutation in ...
3β-Dihydroprogesterone (pregn-4-en-3β-ol-20-one) is an isomer of pregnenolone in which the C5 double bond has been replaced ... 3 (5): 283-90. doi:10.1002/dta.281. PMID 21538944. Sripada RK, Marx CE, King AP, Rampton JC, Ho SS, Liberzon I (2013). " ... 40 (3): 333-6. PMID 1654510. Irwin RP, Maragakis NJ, Rogawski MA, Purdy RH, Farb DH, Paul SM (July 1992). "Pregnenolone sulfate ... Pregnenolone and its 3β-sulfate, pregnenolone sulfate, like DHEA, DHEA sulfate, and progesterone, belong to the group of ...
ISBN 978-0-323-29738-7. Jin Y, Penning TM (2001). "Steroid 5alpha-reductases and 3alpha-hydroxysteroid dehydrogenases: key ... It has an affinity (Kd) of 0.25 to 0.5 nM for the human AR, which is about 2- to 3-fold higher than that of testosterone (Kd = ... 63-. ISBN 978-3-88763-075-1. List PH, Hörhammer L (12 March 2013). Chemikalien und Drogen: Teil B: R, S. Springer-Verlag. pp. ... 3α-Androstanediol is a potent positive allosteric modulator of the GABAA receptor, while 3β-androstanediol is a potent and ...
Retrieved 3 April 2011. de Gier J; Wolthers CH; Galac S; Okkens AC; Kooistra HS (April 2011). "Effects of the 3β-hydroxysteroid ... dehydrogenase inhibitor trilostane on luteal progesterone production in the dog". Theriogenology. 75 (7): 1271-9. doi:10.1016/j ... Retrieved 3 April 2011. Braddock, JA, Church, DB, Robertson, ID, Watson, ADJ (October 2003). "Trilostane treatment in dogs with ... Retrieved 3 April 2011. (PDF) "Treating Cushing's Disease in Dogs". US Food and Drug Administration. Retrieved 3 April 2011. " ...
... alpha-hydroxysteroid dehydrogenase for neurosteroids and its inhibition by benzodiazepines" (pdf). Biol Pharm Bull. 25 (4): 441 ... 113 (1-3): 367-73. doi:10.1016/S0379-0738(00)00226-7. PMID 10978650. Brisse, B.; Tetsch, P.; Toye, A. (1980). "[Clinical study ... Usami N; Yamamoto T; Shintani S; Ishikura S; Higaki Y; Katagiri Y; Hara A. (Apr 2002). "Substrate specificity of human 3(20) ...
154 (3): 1060-1064. doi:10.1016/S0022-5347(01)66976-3. ISSN 0022-5347. Roberts, Alan E.; Ritz, Martha A.; Hoekstra, Susan; ... 11 (3): 101-110. doi:10.1002/(SICI)1522-7146(1996)11:3. 3.0.CO;2-O. ISSN 0887-2082. PMID 9029268. ... ISBN 978-0-8155-1856-3. Dr. Ian Morton; I.K. Morton; Judith M. Hall (31 October 1999). Concise Dictionary of Pharmacological ... Zanoterone does not inhibit 5α-reductase, aromatase, or 3α- or 3β-hydroxysteroid dehydrogenase in vitro. The drug significantly ...
17β-Hydroxysteroid dehydrogenase 2 (17β-HSD2) is an enzyme of the 17β-hydroxysteroid dehydrogenase (17β-HSD) family that in ... dehydrogenase 2". Moeller G, Adamski J (2006). "Multifunctionality of human 17beta-hydroxysteroid dehydrogenases". Mol. Cell. ... Soubhye J, Alard IC, van Antwerpen P, Dufrasne F (2015). "Type 2 17-β hydroxysteroid dehydrogenase as a novel target for the ... In addition to 17β-HSD activity, this enzyme also shows high 20α-hydroxysteroid dehydrogenase activity and can activate the ...
Other names in common use include ketosteroid isomerase (KSI), hydroxysteroid isomerase, steroid isomerase, Δ5-ketosteroid ... In mammals, transfer of a double bond at Δ5 to Δ4 is catalyzed by 3-β-hydroxy-Δ5-steroid dehydrogenase at the same time as the ... A Δ5-3-ketosteroid isomerase-disrupted mutant of strain TA441 can grow on dehydroepiandrosterone, which has a double bond at Δ5 ... 267 (5194): 90-3. doi:10.1126/science.7809611. PMID 7809611. Kraut DA, Sigala PA, Pybus B, Liu CW, Ringe D, Petsko GA, ...
1998). "The identification of 5 alpha-reductase-2 and 17 beta-hydroxysteroid dehydrogenase-3 gene defects in male ... 3-oxo-5α-steroid 4-dehydrogenase 2 is an enzyme that in humans is encoded by the SRD5A2 gene. Steroid 5α-reductase catalyzes ... 80 (3): 269-72. doi:10.1002/(SICI)1096-8628(19981116)80:3. 3.0.CO;2-T. PMID 9843052. Nnane IP, Kato K, Liu Y, et al. (1999). " ... 131 (3): 1571-3. doi:10.1210/en.131.3.1571. PMID 1505484. Andersson S, Berman DM, Jenkins EP, Russell DW (1991). "Deletion of ...
32 (3): 413-20. doi:10.1016/0022-4731(89)90215-X. PMID 2523011. Sippell WG, Dörr HG, Bidlingmaier F, Knorr D (1980). "Plasma ... 12 (3): 287-96. doi:10.1007/BF01811241. PMID 3147727. [non-primary source needed] Martikainen H, Rönnberg L, Ruokonen A, Vihko ... 83 (10): 3750-3. doi:10.1210/jc.83.10.3750. PMID 9768696. Harding CF, Sheridan K, Walters MJ (1983). "Hormonal specificity and ... Raimondi SG, Olivier NS, Patrito LC, Flury A (1989). "Regulation of the 3 beta-hydroxysteroid dehydrogenase activity in tissue ...
138 (3): 911-20. doi:10.1016/j.neuroscience.2005.10.016. PMID 16325348. Eser, D; Romeo, E; Baghai, TC; Di Michele, F; Schüle, C ... 138 (3): 1041-8. doi:10.1016/j.neuroscience.2005.07.007. PMID 16310959. Eser, D; Schüle, C; Baghai, TC; Romeo, E; Rupprecht, R ... 15 (3-4): 197-234. doi:10.1615/critrevneurobiol.v15.i34.20. PMID 15248811. Tuveri, A; Paoletti, AM; Orrù, M; Melis, GB; Marotto ... It is synthesized from the adrenal hormone deoxycorticosterone by the action of two enzymes, 5α-reductase type I and 3α- ...
In patients with congenital adrenal hyperplasia due to 3β-hydroxysteroid dehydrogenase deficiency 17α-hydroxypregnenolone is ... a prohormone for glucocorticosteroids and androstenedione through the activity of 3α-hydroxysteroid dehydrogenase. Measurements ...
... of mirtazapine on plasma concentrations of neuroactive steroids in major depression and on 3alpha-hydroxysteroid dehydrogenase ... "The biological activity of 3alpha-hydroxysteroid oxido-reductase in the spinal cord regulates thermal and mechanical pain ... 29 (3): 339-54. doi:10.1016/s0306-4530(03)00033-7. PMID 14644065. de Wit H, Schmitt L, Purdy R, Hauger R (2001). "Effects of ... 11 (3): 261-72. doi:10.1038/sj.mp.4001782. PMID 16344854. Civic D, Scholes D, Ichikawa L, et al. (June 2000). "Depressive ...
17β-hydroxysteroid dehydrogenase deficiency. *aromatase excess syndrome. *Androgen receptor (Androgen insensitivity syndrome) ... 65 (3): 385-411. doi:10.2165/00003495-200565030-00005. PMID 15669880.. *^ a b c d e f g h i j k l m n o p q r s Melmed, Shlomo ... 3 (4): 722-6. doi:10.1177/193229680900300417. PMC 2769984. PMID 20144319.. *^ a b Selph S, Dana T, Blazina I, Bougatsos C, ... 3-16. ISBN 978-0-387-09840-1. . OCLC 663097550.. *^ a b Koutroumpakis, E; Jozwik, B; Aguilar, D; Taegtmeyer, H (2020). " ...
Mutations in HSD3B2, the gene for 3beta-hydroxysteroid dehydrogenase type II (3beta-HSD II) have been detected and activities ... Mutations in HSD3B2, the gene for 3beta-hydroxysteroid dehydrogenase type II (3beta-HSD II) have been detected and activities ... Phenotypic variability and origins of mutations in the gene encoding 3beta-hydroxysteroid dehydrogenase type II.. Authors:. ... Congenital adrenal hyperplasia due to 3beta-hydroxysteroid dehydrogenase/Delta(5)-Delta(4) isomerase deficiency.Authors: Simard ...
... hydroxysteroid dehydrogenase, bypassing conventional intermediates such as and testosterone, and as such, can ... 3.As to capsules , that would be much easier.You just need to fill the mixture in caps,then you could ... 3.Photo of parcel would be offered for you to tell apart products. No one else would know. about this detail & ... 3:Well-trained and disciplined packing team. Unique ways to ship 10 grams to 100kg powders at one time to your ...
Sinclair PA, Squires EJ: Testicular sulfoconjugation of the 16-androstene steroids by hydroxysteroid sulfotransferase: Its ... Bonneau M, Terqui M: A note on the metabolism of 5α-androst-16-en-3-one in the young boar in vivo. Reprod Nutr Dévelop. 1983, ... Skatole (3-metyl-indole) is a breakdown product of tryptophan. It has a fecal-like odor. Unlike the smell of androstenone the ... 3.. Walstra P, Marse H: Investigation into sex odour of entire male pigs. IVO-Report C-147 (Sept 1970). 30- ...
Mean gonadosomatic index (GSI), however, had increased, probably as a result of ... read more hydration, 3α-Hydroxysteroid ... dehydrogenase (3αHSD), 3βHSD and uridine diphosphoglucose dehydrogenase (UDPGD) reactions were demonstrated in interstitial ... In the testes of spawning fish, total 3βHSD activity was stronger and total UDPGD activity weaker than in prespawning fish, but ... total 3αHSD activity was not different. Plasma gonadotropin (GTH) levels in male catfish were low as compared with females. ...
207-563-3 Epiandrosterone Purity: 99%min Epiandrosterone Appearance: White crystalline powder Epiandrosterone Standard: USP/BP/ ... Epiandrosterone can be converted from the natural steroids androstanediol via17β-hydroxysteroid dehydrogenase or from ... and can also be converted from the natural steroids androstanediol via 17β-hydroxysteroid dehydrogenase or from androstanedione ... Epiandrosterone EINECS: 207-563-3. Epiandrosterone Purity: 99%min. Epiandrosterone Appearance: White crystalline powder. ...
A novel nonstop mutation in the stop codon and a novel missense mutation in the type II 3beta-hydroxysteroid dehydrogenase ( ... Carriers for type II 3beta-hydroxysteroid dehydrogenase (HSD3B2) deficiency can only be identified by HSD3B2 genotype study and ... Simard J, Moisan AM, Morel Y. Congenital adrenal hyperplasia due to 3beta-hydroxysteroid dehydrogenase/Delta(5)-Delta(4) ... Carboxyl-terminal mutations in 3beta-hydroxysteroid dehydrogenase type II cause severe salt-wasting congenital adrenal ...
3-Hydroxysteroid dehydrogenase (3-HSD) may refer to: 3α-Hydroxysteroid dehydrogenase (3α-HSD) 3β-Hydroxysteroid dehydrogenase ( ...
Neville AM, Orr JC, Engel LL (1968). "Delta5-3beta-Hydroxy steroid dehydrogenase activities of bovine adrenal cortex". Biochem ... "Molecular biology of the 3beta-hydroxysteroid dehydrogenase/delta5-delta4 isomerase gene family". Endocr. Rev. 26 (4): 525-82. ... ene steroid dehydrogenase 3β-hydroxy steroid dehydrogenase/isomerase 3β-hydroxy-Δ5-C27-steroid dehydrogenase/isomerase 3β- ... 3β-HSD is also known as delta Δ5-4-isomerase, which catalyzes the oxidative conversion of Δ5-3β-hydroxysteroids to the Δ4-3- ...
cheers, : , ,Max Youll find a lot of information if you search medline with the words : short-chain dehydrogenases. In 1995 ... I would appreciate any leads to literature that cover the structure, : , ,function, kinetics and recent development on 3-beta ... Info required on 3-beta-hydroxy steroid dehydrogenase. Lluis Ribas lluis at aars.mit.edu Thu Sep 26 10:06:28 EST 1996 *Previous ...
The 3-beta-HSD enzymatic system plays a crucial role in the biosynthesis of all classes of hormonal steroids. HSD V can only ... Exhibits only 3-ketosteroid reductase activity in the presence of NADPH and does not function as an isomerase. ... steroid dehydrogenase activity Source: RGD ,p>Traceable Author Statement,/p> ,p>Used for information from review articles where ... 3 beta-hydroxysteroid dehydrogenase type 5Add BLAST. 373. Amino acid modifications. Feature key. Position(s). Description ...
"Newly proposed hormonal criteria via genotypic proof for type II 3beta-hydroxysteroid dehydrogenase deficiency". J. Clin. ... 21 (3): 245-91. doi:10.1210/edrv.21.3.0398. PMID 10857554.. *↑ Hohl A, Ronsoni MF, Oliveira M (2014). "Hirsutism: diagnosis and ... "3-beta-hydroxysteroid dehydrogenase deficiency - Genetics Home Reference".. *↑ Simard J, Rheaume E, Mebarki F, Sanchez R, New ... 3 beta-hydroxysteroid dehydrogenase deficiency must be differentiated from diseases that cause ambiguous genitalia:[2][3] ...
3β-HSD is often associated with steroidogenesis, but its function in the metabolism of both steroids and xenobiotics is more ... 3β-HSD is involved in the synthesis of a number of natural steroid hormones, including progesterone and testosterone, and the ... Much of the research conducted on porcine 3β-HSD is motivated by its importance for the occurrence of the boar taint phenomenon ... This review focuses on the expression and regulation of 3β-hydroxysteroid dehydrogenase/Δ5-Δ4 isomerase (3β-HSD), with emphasis ...
At the core of this process is the placental enzyme 11β-hydroxysteroid dehydrogenase type 2 (11β-HSD2), an enzyme that is ... P. He, Z. Chen, Q. Sun, Y. Li, H. Gu, and X. Ni, "Reduced expression of 11β-hydroxysteroid dehydrogenase type 2 in preeclamptic ... W. Hu, X. Weng, M. Dong, Y. Liu, W. Li, and H. Huang, "Alteration in methylation level at 11β-hydroxysteroid dehydrogenase type ... C. J. Peña, C. Monk, and F. A. Champagne, "Epigenetic effects of prenatal stress on 11β-hydroxysteroid dehydrogenase-2 in the ...
... and 17β-hydroxysteroid dehydrogenase-3 deficiency (17β-HSD-3) are often raised as girls. Over the past number of years, this ... Individuals with 5α-reductase-2 deficiency (5α-RD-2) and 17β-hydroxysteroid dehydrogenase-3 deficiency (17β-HSD-3) are often ... Rösler, A., Silverstein, S., & Abeliovich, D. (1996). A (R80Q) mutation in 17 β-hydroxysteroid dehydrogenase type 3 gene among ... Gender Change in 46,XY Persons with 5α-Reductase-2 Deficiency and 17β-Hydroxysteroid Dehydrogenase-3 Deficiency. ...
Oxidation and isomerization of 3β-hydroxysterols to 4-en-3-ones is requisite for sterol … ... Inhibition of the M. tuberculosis 3β-hydroxysteroid dehydrogenase by azasteroids Bioorg Med Chem Lett. 2011 Apr 15;21(8):2216-9 ... Oxidation and isomerization of 3β-hydroxysterols to 4-en-3-ones is requisite for sterol metabolism and the reaction is ... tb 3β-hydroxysteroid dehydrogenase. 6-Azasteroids with large, hydrophobic side chains at the C17 position are the most ...
3alpha-hydroxy steroid, type 2 3alpha-hydroxysteroid dehydrogenase/type 5 17beta-hydroxysteroid dehydrogenase, type 3 3alpha- ... 3alpha-hydroxysteroid dehydrogenase, 3alpha-hydroxysteroid dehydrogenase/carbonyl reductase, 3alpha-hydroxysteroid oxido- ... hydroxyprostaglandin dehydrogenase, More, NAD(P)+-3alpha-hydroxysteroid dehydrogenase, NAD+-dependent 3alpha-HSD, NADP(H)- ... 3alpha/3beta-hydroxysteroid dehydrogenase, 3alphaHSD, 3HSD, 5alpha-dihydroprogesterone 3alpha-hydroxysteroid oxidoreductase, ...
... see under 17-HYDROXYSTEROID DEHYDROGENASES (85-90); on-line search 17-HYDROXYSTEROID DEHYDROGENASES (85-93), Index Medicus ... beta-hydroxysteroid dehydrogenase: acts on both 3 beta or 17 beta hydroxysteroids; 17 beta type 1 is probably ESTRADIOL ... DEHYDROGENASES; for 3 or 17 alpha-hydroxysteroids see EC 1.1.1.209; was mapped to TESTOSTERONE DEHYDRONGENASES (85-93) ( ... Hydroxysteroid Dehydrogenases: 6*17-Hydroxysteroid Dehydrogenases: 4*3 (or 17)-beta-hydroxysteroid dehydrogenase: 145 ...
3-beta-HSD is a bifunctional enzyme, that catalyzes the oxidative conversion of Delta(5)-ene-3-beta-hydroxy steroid, and the ... The 3-beta-HSD enzymatic system plays a crucial role in the biosynthesis of all classes of hormonal steroids. ... 3-beta-HSD is a bifunctional enzyme, that catalyzes the oxidative conversion of Delta5-ene-3-beta-hydroxy steroid, and the ... The 3-beta-HSD enzymatic system plays a crucial role in the biosynthesis of all classes of hormonal steroids. ...
Crystal structure of human type III 3alpha-hydroxysteroid dehydrogenase/bile acid binding protein complexed with NADP(+) and ... 3] Andreeva A., Howorth D., Chandonia J.-M., Brenner S.E., Hubbard T.J.P., Chothia C., Murzin A.G. (2008).. Data growth and its ... Description: 3-ALPHA-HYDROXYSTEROID DEHYDROGENASE protein , Length: 323 No structure alignment results are available for 1IHI.A ... If available, the SCOP 1.75 domain assignment [3] is used. Otherwise algorithmic domain assignments are computed using the ...
... crystal structure of testosterone and NADP+ bound to 3 alpha-hydroxysteroid/dihydrodiol dehydrogenase. ... 3-ALPHA-HYDROXYSTEROID DEHYDROGENASE protein, length: 323 (BLAST) Sequence Similarity Cutoff. Rank. Chains in Cluster. Cluster ... RECOMBINANT RAT LIVER 3-ALPHA-HYDROXYSTEROID DEHYDROGENASE (3-ALPHA-HSD) COMPLEXED WITH NADP AND TESTOSTERONE. ...
... is identified with human liver dihydrodiol dehydrogenase isoform 1 that exhibits high 20α-hydroxysteroid dehydrogenase and very ... hydroxysteroid dehydrogenase from human prostatic cytosol. J Steroid Biochem Mol Biol 42:321-327. ... Lineweaver-Burk analysis of the dual effects of clofibric acid on the dehydrogenase activity of AKR 1C4. In A and B, the ... 1990) Purification and properties of multiple forms of dihydrodiol dehydrogenase from human liver. J Biochem (Tokyo) 108:250- ...
3-alpha hydroxysteroid dehydrogenase, type II)), Authors: Hsueh Kung Lin. Published in: Atlas Genet Cytogenet Oncol Haematol. ... Increased expression of type 2 3alpha-hydroxysteroid dehydrogenase/type 5 17beta-hydroxysteroid dehydrogenase (AKR1C3) and its ... Localization of type 5 17beta-hydroxysteroid dehydrogenase, 3beta-hydroxysteroid dehydrogenase, and androgen receptor in the ... Immunoelectron microscopic localization of 3beta-hydroxysteroid dehydrogenase and type 5 17beta-hydroxysteroid dehydrogenase in ...
Read about 3 beta hydroxysteroid dehydrogenase deficiency medical facts: what is the definition of 3 beta hydroxysteroid ... Read about 3 beta hydroxysteroid dehydrogenase deficiency medical facts: what is the definition of 3 beta hydroxysteroid ... dehydrogenase deficiency, pathophysiology, medical care, frequency, mortality or morbidity, and related 3 beta hydroxysteroid ... dehydrogenase deficiency, pathophysiology, medical care, frequency, mortality or morbidity, and related 3 beta hydroxysteroid ...
The enzyme 3beta/17beta-hydroxysteroid dehydrogenase (3beta/17beta-HSD) is a steroid-inducible component of the Gram-negative ... The active site contains a Ser-Tyr-Lys triad, typical for short-chain dehydrogenases/reductases (SDR). Despite their highly ... Structure of bacterial 3 beta/17 beta-hydroxysteroid dehydrogenase at 1.2 angstrom resolution: A model for multiple steroid ... It catalyzes the reversible reduction/ dehydrogenation of the oxo/beta-hydroxy groups at positions 3 and 17 of steroid ...
... Common Name(s). 17-Beta hydroxysteroid dehydrogenase 3 deficiency, 17-Beta ... 17-beta hydroxysteroid dehydrogenase 3 deficiency is caused by mutations in the HSD17B3 gene and is inherited in an autosomal ... 17-beta hydroxysteroid dehydrogenase 3 deficiencyis an inherited condition that affects male sexual development. People with ... Please click this link to visit the PubMed website for results on "17-Beta hydroxysteroid dehydrogenase 3 deficiency". ...
  • Two substances are the main contributors to boar taint in pork from entire male pigs i.e. the steroid androstenone (5α-androst-16-ene-3-one) [ 1 ] and skatole (3-methyl-indole) [ 2 , 3 ]. (beds.ac.uk)
  • A steroid hormone that is present in normal human urine as a minor constituent , it is a less active 3β-isomer of the androgen Androsterone (A635535). (passionchemical.com)
  • In the testes of spawning fish, total 3βHSD activity was stronger and total UDPGD activity weaker than in prespawning fish, but total 3αHSD activity was not different. (uu.nl)
  • Medroxyprogesterone acetate and medrogestone are weak inhibitors of 3β-HSD which may substantially inhibit it at high dosages. (wikipedia.org)
  • In addition, analyses of several commonly used UV-filters on estrogen- and androgen-metabolizing 17beta-HSD enzymes revealed 3-benzylidene camphor (3-BC) and 4-methylbenzylidene camphor (4-MBC) as low micromolar 17beta-HSD2 inhibitors. (unibas.ch)
  • The amounts of testosterone and 11-KT were measured in incubation media after 24 h of exposure of testis explants at stage I-II or III to 100 ng/ml of rFsh and rLh, in the presence or absence of 5 uM of inhibitors of the cAMP/PKA pathway (MDL and H-89 respectively) and Hsd-3β (TRIL). (selleckchem.com)
  • The 3β-HSD complex is responsible for the conversion of: Pregnenolone to progesterone 17α-Hydroxypregnenolone to 17α-hydroxyprogesterone DHEA to androstenedione Androstenediol to testosterone Androstadienol to androstadienone 3β-HSD belongs to the family of oxidoreductases, to be specific, those acting on the CH-OH group with NAD+ or NADP+ as acceptor. (wikipedia.org)
  • AKR1C3 metabolizes various androgen metabolites including 5a-dihydrotestosterone to 5a-androstane-3a,17b-diol, Delta 4 -androstene-3,17-dione to testosterone, androstanedione to 5a-dihydrotestosterone, androsterone to 5a-androstane-3a,17b-diol. (atlasgeneticsoncology.org)
  • 17 beta-hydroxysteroid dehydrogenase 3 deficiency consists of a defect in the last phase of steroidogenesis, in which androstenedione is converted into testosterone and estrone into estradiol. (usp.br)
  • Elevated LH of 24 mIU/L and FSH of 36 mIU/mL with elevated testosterone of 3 ng/mL (normal range for male, 2.4 8.3) were found. (eurospe.org)
  • StAR, P450scc and 3β-HSD expression in the Leydig cells of the testis were also higher during this season, as was serum testosterone. (scielo.cl)
  • In the developed testis, Leydig cells (LCs) maintain high levels of P450scc and 3β-HSD and, in response to luteinizing hormone (LH), rapidly synthesize StAR and testosterone [ 15 , 16 ]. (scielo.cl)
  • At about 1 week of age, gonadotropin and testosterone levels begin to rise to pubertal levels, peaking at age 1-3 months, and then decreasing to prepubertal levels by age 6 months. (medscape.com)
  • In both normal glandular and carcinomatous breast tissue, the concentrations of androstenedione (A), dehydroepiandrosterone (DHEA), 5 androstene-3 beta, 17 beta-diol (5-Adiol), estrone (E1), estradiol (E2) and progesterone (P) were significantly higher than plasma concentrations. (nih.gov)
  • The present study further provides the first immunocytochemical mapping of the site of 3βHSD expression in the fish CNS. (elsevier.com)
  • Our interpretation of the available crystal structure of 3 alpha/20 beta-HSD from Streptomyces hydrogenans suggests a hydrogen bond in that enzyme between the Thr12 side chain and the backbone NH of Asn87 rather than the coenzyme, indicating that this hydrogen bond to the beta D strand might determine a crucial difference between the reductive and the oxidative reaction types. (ox.ac.uk)
  • The influence of fixation on the activity pattern, the possible diffusion of enzyme, the nothing dehydrogenase reaction, and the substantivity of the tetrazolium salts and formazans were investigated in control experiments. (springer.com)
  • Prior research has suggested that musk gland development and function might be regulated by androgens [ 2 , 3 ] produced by the testis under the control of the hypothalamus-pituitary-testis system [ 4 , 5 ]. (scielo.cl)