Cholesterol Oxidase: An enzyme that catalyzes the oxidation of cholesterol in the presence of molecular oxygen to 4-cholesten-3-one and hydrogen peroxide. The enzyme is not specific for cholesterol, but will also oxidize other 3-hydroxysteroids. EC 1.1.3.6.5-alpha Reductase Inhibitors: Drugs that inhibit 3-OXO-5-ALPHA-STEROID 4-DEHYDROGENASE. They are commonly used to reduce the production of DIHYDROTESTOSTERONE.Cholestenone 5 alpha-Reductase: An oxidoreductase that catalyzes the conversion of 3-oxo-delta4 steroids into their corresponding 5alpha form. It plays an important role in the conversion of TESTOSTERONE into DIHYDROTESTOSTERONE and PROGESTERONE into DIHYDROPROGESTERONE.Azasteroids: Steroidal compounds in which one or more carbon atoms in the steroid ring system have been substituted with nitrogen atoms.Finasteride: An orally active 3-OXO-5-ALPHA-STEROID 4-DEHYDROGENASE inhibitor. It is used as a surgical alternative for treatment of benign PROSTATIC HYPERPLASIA.3-Oxo-5-alpha-Steroid 4-Dehydrogenase: An enzyme that catalyzes the reduction of TESTOSTERONE to 5-ALPHA DIHYDROTESTOSTERONE.Urinary Retention: Inability to empty the URINARY BLADDER with voiding (URINATION).Oxidoreductases Acting on CH-CH Group Donors: A subclass of enzymes which includes all dehydrogenases acting on carbon-carbon bonds. This enzyme group includes all the enzymes that introduce double bonds into substrates by direct dehydrogenation of carbon-carbon single bonds.Prostatic Hyperplasia: Increase in constituent cells in the PROSTATE, leading to enlargement of the organ (hypertrophy) and adverse impact on the lower urinary tract function. This can be caused by increased rate of cell proliferation, reduced rate of cell death, or both.Nitrate Reductases: Oxidoreductases that are specific for the reduction of NITRATES.Hydroxymethylglutaryl CoA Reductases: Enzymes that catalyze the reversible reduction of alpha-carboxyl group of 3-hydroxy-3-methylglutaryl-coenzyme A to yield MEVALONIC ACID.Ribonucleotide ReductasesCytochrome-B(5) Reductase: A FLAVOPROTEIN oxidoreductase that occurs both as a soluble enzyme and a membrane-bound enzyme due to ALTERNATIVE SPLICING of a single mRNA. The soluble form is present mainly in ERYTHROCYTES and is involved in the reduction of METHEMOGLOBIN. The membrane-bound form of the enzyme is found primarily in the ENDOPLASMIC RETICULUM and outer mitochondrial membrane, where it participates in the desaturation of FATTY ACIDS; CHOLESTEROL biosynthesis and drug metabolism. A deficiency in the enzyme can result in METHEMOGLOBINEMIA.Nitrite Reductases: A group of enzymes that oxidize diverse nitrogenous substances to yield nitrite. (Enzyme Nomenclature, 1992) EC 1.Glutathione Reductase: Catalyzes the oxidation of GLUTATHIONE to GLUTATHIONE DISULFIDE in the presence of NADP+. Deficiency in the enzyme is associated with HEMOLYTIC ANEMIA. Formerly listed as EC 1.6.4.2.FMN Reductase: An enzyme that utilizes NADH or NADPH to reduce FLAVINS. It is involved in a number of biological processes that require reduced flavin for their functions such as bacterial bioluminescence. Formerly listed as EC 1.6.8.1 and EC 1.5.1.29.Thioredoxin-Disulfide Reductase: A FLAVOPROTEIN enzyme that catalyzes the oxidation of THIOREDOXINS to thioredoxin disulfide in the presence of NADP+. It was formerly listed as EC 1.6.4.5NADPH-Ferrihemoprotein Reductase: A flavoprotein that catalyzes the reduction of heme-thiolate-dependent monooxygenases and is part of the microsomal hydroxylating system. EC 1.6.2.4.Ferredoxin-NADP Reductase: An enzyme that catalyzes the oxidation and reduction of FERREDOXIN or ADRENODOXIN in the presence of NADP. EC 1.18.1.2 was formerly listed as EC 1.6.7.1 and EC 1.6.99.4.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)Cytochrome Reductasesalpha 1-Antitrypsin: Plasma glycoprotein member of the serpin superfamily which inhibits TRYPSIN; NEUTROPHIL ELASTASE; and other PROTEOLYTIC ENZYMES.Tetrahydrofolate Dehydrogenase: An enzyme of the oxidoreductase class that catalyzes the reaction 7,8-dihyrofolate and NADPH to yield 5,6,7,8-tetrahydrofolate and NADPH+, producing reduced folate for amino acid metabolism, purine ring synthesis, and the formation of deoxythymidine monophosphate. Methotrexate and other folic acid antagonists used as chemotherapeutic drugs act by inhibiting this enzyme. (Dorland, 27th ed) EC 1.5.1.3.Methylenetetrahydrofolate Reductase (NADPH2): A flavoprotein amine oxidoreductase that catalyzes the reversible conversion of 5-methyltetrahydrofolate to 5,10-methylenetetrahydrofolate. This enzyme was formerly classified as EC 1.1.1.171.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.Nitrate Reductase (NADH): An NAD-dependent enzyme that catalyzes the oxidation of nitrite to nitrate. It is a FLAVOPROTEIN that contains IRON and MOLYBDENUM and is involved in the first step of nitrate assimilation in PLANTS; FUNGI; and BACTERIA. It was formerly classified as EC 1.6.6.1.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)Methionine Sulfoxide Reductases: Reductases that catalyze the reaction of peptide-L-methionine -S-oxide + thioredoxin to produce peptide-L-methionine + thioredoxin disulfide + H(2)O.Receptors, Adrenergic, alpha: One of the two major pharmacological subdivisions of adrenergic receptors that were originally defined by the relative potencies of various adrenergic compounds. The alpha receptors were initially described as excitatory receptors that post-junctionally stimulate SMOOTH MUSCLE contraction. However, further analysis has revealed a more complex picture involving several alpha receptor subtypes and their involvement in feedback regulation.Kinetics: The rate dynamics in chemical or physical systems.Ribonucleoside Diphosphate Reductase: An enzyme of the oxidoreductase class that catalyzes the formation of 2'-deoxyribonucleotides from the corresponding ribonucleotides using NADPH as the ultimate electron donor. The deoxyribonucleoside diphosphates are used in DNA synthesis. (From Dorland, 27th ed) EC 1.17.4.1.Hydroxymethylglutaryl-CoA Reductase Inhibitors: Compounds that inhibit HMG-CoA reductases. They have been shown to directly lower cholesterol synthesis.Quinone Reductases: NAD(P)H:(quinone acceptor) oxidoreductases. A family that includes three enzymes which are distinguished by their sensitivity to various inhibitors. EC 1.6.99.2 (NAD(P)H DEHYDROGENASE (QUINONE);) is a flavoprotein which reduces various quinones in the presence of NADH or NADPH and is inhibited by dicoumarol. EC 1.6.99.5 (NADH dehydrogenase (quinone)) requires NADH, is inhibited by AMP and 2,4-dinitrophenol but not by dicoumarol or folic acid derivatives. EC 1.6.99.6 (NADPH dehydrogenase (quinone)) requires NADPH and is inhibited by dicoumarol and folic acid derivatives but not by 2,4-dinitrophenol.Hypoxia-Inducible Factor 1, alpha Subunit: Hypoxia-inducible factor 1, alpha subunit is a basic helix-loop-helix transcription factor that is regulated by OXYGEN availability and is targeted for degradation by VHL TUMOR SUPPRESSOR PROTEIN.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).NADH, NADPH Oxidoreductases: A group of oxidoreductases that act on NADH or NADPH. In general, enzymes using NADH or NADPH to reduce a substrate are classified according to the reverse reaction, in which NAD+ or NADP+ is formally regarded as an acceptor. This subclass includes only those enzymes in which some other redox carrier is the acceptor. (Enzyme Nomenclature, 1992, p100) EC 1.6.Base Sequence: The sequence of PURINES and PYRIMIDINES in nucleic acids and polynucleotides. It is also called nucleotide sequence.Dihydropteridine Reductase: An enzyme that catalyzes the reduction of 6,7-dihydropteridine to 5,6,7,8-tetrahydropteridine in the presence of NADP+. Defects in the enzyme are a cause of PHENYLKETONURIA II. Formerly listed as EC 1.6.99.7.Oxidation-Reduction: A chemical reaction in which an electron is transferred from one molecule to another. The electron-donating molecule is the reducing agent or reductant; the electron-accepting molecule is the oxidizing agent or oxidant. Reducing and oxidizing agents function as conjugate reductant-oxidant pairs or redox pairs (Lehninger, Principles of Biochemistry, 1982, p471).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.Thioredoxin Reductase 1: A subtype of thioredoxin reductase found primarily in the CYTOSOL.Enoyl-(Acyl-Carrier-Protein) Reductase (NADH): An NAD-dependent enzyme that catalyzes the oxidation of acyl-[acyl-carrier protein] to trans-2,3-dehydroacyl-[acyl-carrier protein]. It has a preference for acyl groups with a carbon chain length between 4 to 16.Protein S: The vitamin K-dependent cofactor of activated PROTEIN C. Together with protein C, it inhibits the action of factors VIIIa and Va. A deficiency in protein S; (PROTEIN S DEFICIENCY); can lead to recurrent venous and arterial thrombosis.Search Engine: Software used to locate data or information stored in machine-readable form locally or at a distance such as an INTERNET site.Databases, Genetic: Databases devoted to knowledge about specific genes and gene products.Genome, Human: The complete genetic complement contained in the DNA of a set of CHROMOSOMES in a HUMAN. The length of the human genome is about 3 billion base pairs.PubMed: A bibliographic database that includes MEDLINE as its primary subset. It is produced by the National Center for Biotechnology Information (NCBI), part of the NATIONAL LIBRARY OF MEDICINE. PubMed, which is searchable through NLM's Web site, also includes access to additional citations to selected life sciences journals not in MEDLINE, and links to other resources such as the full-text of articles at participating publishers' Web sites, NCBI's molecular biology databases, and PubMed Central.Periodicals as Topic: A publication issued at stated, more or less regular, intervals.Sebaceous Glands: Small, sacculated organs found within the DERMIS. Each gland has a single duct that emerges from a cluster of oval alveoli. Each alveolus consists of a transparent BASEMENT MEMBRANE enclosing epithelial cells. The ducts from most sebaceous glands open into a HAIR FOLLICLE, but some open on the general surface of the SKIN. Sebaceous glands secrete SEBUM.BooksPublishing: "The business or profession of the commercial production and issuance of literature" (Webster's 3d). It includes the publisher, publication processes, editing and editors. Production may be by conventional printing methods or by electronic publishing.MEDLINE: The premier bibliographic database of the NATIONAL LIBRARY OF MEDICINE. MEDLINE® (MEDLARS Online) is the primary subset of PUBMED and can be searched on NLM's Web site in PubMed or the NLM Gateway. MEDLINE references are indexed with MEDICAL SUBJECT HEADINGS (MeSH).Serial Publications: Publications in any medium issued in successive parts bearing numerical or chronological designations and intended to be continued indefinitely. (ALA Glossary of Library and Information Science, 1983, p203)

Reversion of the differentiated phenotype and maturation block in Sertoli cells in pathological human testis. (1/92)

To study the relationship between abnormal Sertoli cell differentiation and spermatogenic impairment, we examined the expression of Sertoli cell markers normally lost at puberty, cytokeratin 18 (CK18), anti-Mullerian hormone (AMH) and M2A antigen, in three children (aged 1-2 years), 50 adults (aged 19-45 years) with obstructive or non-obstructive azoospermia or oligozoospermia, and six patients (aged 1-18 years) with 5 alpha-reductase deficiency. There was CK18 and/or AMH expression, but never M2A antigen expression, associated with spermatogonial arrest or Sertoli cell-only (SCO) syndrome in infertile men. Loss of M2A antigen suggests the transition of Sertoli cells to an adult phenotype, while CK18 and/or AMH expression may be a manifestation of de-differentiation of Sertoli cells. In 5 alpha-reductase deficiency, there was a sequential loss of CK18, M2A antigen and AMH around puberty, associated with partial spermatogenesis. The persistence of immature Sertoli cells expressing M2A antigen was associated with prepubertal seminiferous cords and SCO syndrome. Therefore, 5 alpha-reductase deficiency may prevent the maturation of Sertoli cells, resulting in impairment of spermatogenesis, and loss of M2A antigen expression coincides with a critical step in the Sertoli cell maturation. High follicle stimulating hormone concentrations due to failure of normal Sertoli cell differentiation indicate a normal development pattern of the hypothalamic-pituitary-gonadal axis.  (+info)

Selective serotonin reuptake inhibitors directly alter activity of neurosteroidogenic enzymes. (2/92)

The neurosteroid 3alpha-hydroxysteroid-5alpha-pregnan-20-one (allopregnanolone) acts as a positive allosteric modulator of gamma-aminobutyric acid at gamma-aminobutyric acid type A receptors and hence is a powerful anxiolytic, anticonvulsant, and anesthetic agent. Allopregnanolone is synthesized from progesterone by reduction to 5alpha-dihydroprogesterone, mediated by 5alpha-reductase, and by reduction to allopregnanolone, mediated by 3alpha-hydroxysteroid dehydrogenase (3alpha-HSD). Previous reports suggested that some selective serotonin reuptake inhibitors (SSRIs) could alter concentrations of allopregnanolone in human cerebral spinal fluid and in rat brain sections. We determined whether SSRIs directly altered the activities of either 5alpha-reductase or 3alpha-HSD, using an in vitro system containing purified recombinant proteins. Although rats appear to express a single 3alpha-HSD isoform, the human brain contains several isoforms of this enzyme, including a new isoform we cloned from human fetal brains. Our results indicate that the SSRIs fluoxetine, sertraline, and paroxetine decrease the K(m) of the conversion of 5alpha-dihydroprogesterone to allopregnanolone by human 3alpha-HSD type III 10- to 30-fold. Only sertraline inhibited the reverse oxidative reaction. SSRIs also affected conversions of androgens to 3alpha- and 3alpha, 17beta-reduced or -oxidized androgens mediated by 3alpha-HSD type II(Brain). Another antidepressant, imipramine, was without any effect on allopregnanolone or androstanediol production. The region-specific expression of 3alpha-HSD type II(Brain) and 3alpha-HSD type III mRNAs suggest that SSRIs will affect neurosteroid production in a region-specific manner. Our results may thus help explain the rapid alleviation of the anxiety and dysphoria associated with late luteal phase dysphoria disorder and major unipolar depression by these SSRIs.  (+info)

2,3,7,8-tetrachlorodibenzo-p-dioxin inhibits luminal cell differentiation and androgen responsiveness of the ventral prostate without inhibiting prostatic 5alpha-dihydrotestosterone formation or testicular androgen production in rat offspring. (3/92)

In utero and lactational exposure to a single maternal dose of 1 microg 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)/kg causes some overt toxicity and impairs prostate growth in male offspring. As similar effects on the ventral prostate can be caused by decreased testosterone production during perinatal development, we determined whether intratesticular testosterone content, testicular responsiveness to gonadotropin stimulation, or plasma testosterone concentrations were reduced in fetal and newborn rats. Because these endpoints were not affected, the ability of TCDD exposure to inhibit synthesis of the proximal androgen in prostate development, 5alpha-dihydrotestosterone (DHT), from the circulating precursor testosterone and 5alpha-androstane-3alpha,17ss-diol (3alpha-Diol), was studied on postnatal days (PNDs) 14, 21, and 32. The ability of the ventral prostate to form DHT from 3alpha-Diol was slightly impaired on PND 14, but this transient effect was not statistically significant, and recovery was evident by PND 21. Subsequent experiments used organ culture to study the effects of in vivo TCDD exposure on androgen metabolism, androgen responsiveness, androgen receptor expression, and luminal epithelial cell differentiation after in vitro exposure to graded androgen concentrations. In utero and lactational TCDD exposure had no effect on DHT formation in organ culture, but transiently reduced the androgen -induced expression of prostatic-binding protein subunit C3, decreased ventral prostate epithelial cell androgen receptor expression, and inhibited the formation of androgen responsive luminal epithelial cells. These results suggest that TCDD exposure impairs prostate growth and androgen responsiveness by inhibiting prostatic epithelial cell differentiation.  (+info)

Sebocytes are the key regulators of androgen homeostasis in human skin. (4/92)

The mRNA expression patterns of the androgen receptor and the androgen metabolizing enzymes 3beta-hydroxysteroid dehydrogenase/Delta(5-4)-isomerase, 17beta-hydroxysteroid dehydrogenase, 5alpha-reductase, and 3alpha-hydroxysteroid dehydrogenase were investigated in three different cell populations originating from human skin, SZ95 sebocytes, HaCaT keratinocytes, and MeWo melanoma cells, by means of reverse transcription polymerase chain reaction. Restriction analysis of cDNA fragments was performed to identify isozymes of 3beta-hydroxysteroid dehydrogenase/Delta(5-4)-isomerase and 3alpha-hydroxysteroid dehydrogenase. In addition, 3H-dihydroepiandrosterone and 3H-testosterone were used as substrates to determine the metabolic activity of these enzymes in SZ95 sebocytes, primary sebocyte cultures, and HaCaT keratinocytes. Furthermore, the effects of the selective 5alpha-reductase type 1 and 2 inhibitors, 4,7beta-dimethyl-4-aza-5alpha-cholestan-3-one and dihydrofinasteride, respectively, and of the 3beta-hydroxysteroid dehydrogenase/Delta(5-4)-isomerase inhibitor cyproterone acetate on androgen metabolism were investigated. Androgen receptor mRNA was detected in SZ95 sebocytes and HaCaT keratinocytes but not in MeWo melanoma cells, whereas 3beta-hydroxysteroid dehydrogenase/Delta(5-4)-isomerase isotype 1 mRNA and metabolic activity were only found in SZ95 sebocytes. The enzyme activity could be inhibited by cyproterone acetate. Type 2 17beta-hydroxysteroid dehydrogenase, type 1 5alpha-reductase, and 3alpha-hydroxysteroid dehydrogenase mRNA were expressed in all three cell populations tested, whereas type 3 17beta-hydroxysteroid dehydrogenase mRNA could only be detected in SZ95 sebocytes. The major metabolic steps of testosterone in SZ95 sebocytes, primary sebocyte cultures, and HaCaT keratinocytes were its conversion to androstenedione by 17beta-hydroxysteroid dehydrogenase and further to 5alpha-androstanedione by 5alpha-reductase. The type 1 5alpha-reductase selective inhibitor 4,7beta-dimethyl-4-aza-5alpha-cholestan-3-one, but not the type 2 selective inhibitor dihydrofinasteride, inhibited 5alpha-reductase at low concentrations in SZ95 sebocytes and HaCaT keratinocytes. 5alpha-androstanedione was degraded to androsterone by 3alpha-hydroxysteroid dehydrogenase, which exhibited a stronger activity in HaCaT keratinocytes than in SZ95 sebocytes and in primary sebocyte cultures. Lower levels of 5alpha-dihydrotestosterone and 5alpha-androstanediol were also detected in all cells tested. Our investigations show that specific enzyme expression and activity in cultured sebocytes and keratinocytes seem to allocate different duties to these cells in vitro. Sebocytes are able to synthesize testosterone from adrenal precursors and to inactivate it in order to maintain androgen homeostasis, whereas keratinocytes are responsible for androgen degradation.  (+info)

Lifestyle determinants of 5alpha-reductase metabolites in older African-American, white, and Asian-American men. (5/92)

Men with higher endogenous 5alpha-reductase activity may have higher prostate cancer risk. This hypothesis raises two questions: (a) Could racial differences in 5alpha-reductase activity explain the observed racial differences in prostate cancer risk? and (b) Could a man reduce his activity level by modifying his lifestyle? To address these questions, we measured two hormonal indices of 5alpha-reductase activity [serum levels of androstane-3alpha-17beta-diol glucuronide (3alpha-diol G) and androsterone glucuronide (AG)] in healthy, older African-American, white, and Asian-American men, who are at high, intermediate, and low prostate cancer risk, respectively. We also examined associations between these metabolite levels and such lifestyle characteristics as body size and physical activity as well as select aspects of medical history and family history of prostate cancer. Men included in this cross-sectional analysis (n = 1054) had served as control subjects in a population-based case-control study of prostate cancer we conducted in California, Hawaii, and Vancouver, Canada and provided information on certain personal attributes and donated blood between March 1990 and March 1992. In this study, concentrations of 3alpha-diol G declined significantly with age and increased significantly with body mass index. Mean levels of 3alpha-diol G, adjusted for age and body mass index, were 6.1 ng/ml in African-Americans, 6.9 ng/ml in whites and 4.8 ng/ml in Asian-Americans. These differences were statistically significant (African-Americans versus whites: P < 0.01; whites versus Asian-Americans: P < 0.001). Concentrations of AG decreased significantly with age, but only in whites, and were unrelated to any of the reported personal attributes. Mean levels of AG, adjusted for age, were 44.1 ng/ml in African-Americans, 44.9 ng/ml in whites, and 37.5 ng/ml in Asian-Americans (Asian-Americans versus whites, P < 0.001). In conclusion, older African-American and white men have similar levels of these two indices of 5alpha-reductase activity, and these levels are higher than those of older Asian-American men. This difference may be related to the lower prostate cancer risk in Asian-Americans.  (+info)

Dietary soy-phytoestrogens decrease testosterone levels and prostate weight without altering LH, prostate 5alpha-reductase or testicular steroidogenic acute regulatory peptide levels in adult male Sprague-Dawley rats. (6/92)

Nutritional factors, especially phytoestrogens, have been extensively studied for their potential beneficial effects against hormone-dependent and age-related diseases. The present study describes the short-term effects of dietary phytoestrogens on regulatory behaviors (food/water intake, locomotor activity and body weight), prostate weight, prostate 5alpha-reductase enzyme activity, reproductive hormone levels, and testicular steroidogenic acute regulatory peptide (StAR) levels in adult Sprague-Dawley rats. Animals were fed either a phytoestrogen-rich diet containing approximately 600 microg/g isoflavones (as determined by HPLC) or a phytoestrogen-free diet. After 5 weeks of consuming these diets, plasma phytoestrogen levels were 35 times higher in animals fed the phytoestrogen-rich vs phytoestrogen-free diets. Body and prostate weights were significantly decreased in animals fed the phytoestrogen-rich diet vs the phytoestrogen-free fed animals; however, no significant change in prostate 5alpha-reductase enzyme activity was observed between the treatment groups. Locomotor activity levels were higher in the phytoestrogen-rich vs the phytoestrogen-free animals during the course of the treatment interval. Plasma testosterone and androstenedione levels were significantly lower in the animals fed the phytoestrogen-rich diet compared with animals fed the phytoestrogen-free diet. However, there were no significant differences in plasma LH or estradiol levels between the diet groups. Testicular StAR levels were not significantly different between the phytoestrogen-rich vs the phytoestrogen-free fed animals. These results indicated that consumption of dietary phytoestrogens resulting in very high plasma isoflavone levels over a relatively short period can significantly alter body and prostate weight and plasma androgen hormone levels without affecting gonadotropin or testicular StAR levels. The findings of this study identify the biological actions of phytoestrogens on male reproductive endocrinology and provide insights into the protective effects these estrogen mimics exert in male reproductive disorders such as benign prostatic hyperplasia and prostate cancer.  (+info)

Polymorphic markers in the SRD5A2 gene and prostate cancer risk: a population-based case-control study. (7/92)

It has been suggested that the activity of the steroid 5alpha-reductase type II enzyme (encoded by the SRD5A2 gene) may be associated with prostate cancer risk and that population differences in this enzyme's activity may account for part of the substantial racial/ethnic disparity in prostate cancer risk. To provide etiological clues, we evaluated the relationships of four polymorphic markers in the SRD5A2 gene, specifically, A49T (a substitution of threonine for alanine at codon 49), V89L (a substitution of leucine for valine at codon 89), R227Q (a substitution of glutamine for arginine at codon 227), and a (TA)n dinucleotide repeat, with prostate cancer risk in a population-based case-control study in China, a population with the lowest reported prostate cancer incidence rate in the world. Genotypes of these four markers were determined from genomic DNA of 191 incident cases of prostate cancer and 304 healthy controls using PCR-based assays, and serum androgen levels were measured in relation to these genotypes. All study subjects had the wild-type AA genotype of the A49T marker, and 99% had the RR genotype of the R227Q marker. For the V89L marker, prevalences of the LL, VV, and VL genotypes among controls were 35%, 21%, and 45%, respectively. Compared with men with the VV genotype, those with the LL genotype had a statistically nonsignificant 12% reduced risk (odds ratio = 0.88, 95% confidence interval, 0.53-1.47). In addition, men with the LL genotype had significantly higher serum levels of testosterone and significantly lower serum levels of 5alpha-androstane-3alpha,17beta-diol glucuronide than men with other genotypes. Men heterozygous for the (TA)0 allele of the (TA)n marker had a modest, statistically nonsignificant risk reduction (odds ratio = 0.67; 95% confidence interval, 0.39-1.12) compared with men homozygous for the (TA)0 allele, along with significantly higher serum dihydrotestosterone levels. The observed V89L genotype prevalences and the association between V89L genotypes and serum androgen levels support the hypothesis that genotypes associated with lower levels of 5alpha-reductase activity are more common in low-risk populations. Although we found no statistically significant associations of these SRD5A2 polymorphisms with prostate cancer risk, a small effect of these markers cannot be ruled out because of the rarity of certain marker genotypes. Larger studies are needed to further clarify the role of these markers and to elucidate whether genetic diversity of the SRD5A2 gene, alone or in combination with other susceptibility genes, can help explain the large racial/ethnic differences in prostate cancer risk.  (+info)

Allelic frequencies of six polymorphic markers for risk of prostate cancer. (8/92)

The aim of the present study was to evaluate the distribution of polymorphisms for the androgen receptor (AR) (CAG, StuI, GGN), SRD5A2 (Ala49Thr, Val89Leu) and CYP17 (MspA1) genes that are considered to be relevant for risk of prostate cancer. We studied 200 individuals from two cities in the State of Sao Paulo, by PCR, PCR-RFLP and ASOH techniques. The allelic frequencies of the autosomal markers and the StuI polymorphism of the AR gene were very similar to those described in most North American and European populations. In relation to the CAG and GGN number of repeats, the study subjects had smaller repeat lengths (mean of 20.65 and 22.38, respectively) than those described in North American, European and Chinese populations. In the present study, 30.5% of the individuals had less than 22 CAG repeats and 45.5% had less than 23 GGN repeats. When both repeat lengths are considered jointly, this Brazilian population is remarkably different from the others. Further studies on prostate cancer patients need to be conducted to assess the significance of these markers in the Brazilian population.  (+info)

Changes in the voice are almost always indicative of a medical problem; patients experiencing hoarseness or other voice changes should see a physician to determine the cause
Looking for online definition of 5-alpha-reductase in the Medical Dictionary? 5-alpha-reductase explanation free. What is 5-alpha-reductase? Meaning of 5-alpha-reductase medical term. What does 5-alpha-reductase mean?
Prospective studies suggest that prostate cancer risk may be increased in association with high serum concentrations of free testosterone and androstanediol glucuronide (A-diol-g). Polymorphisms have been identified in the 17-hydroxylase cytochrome P450 gene (CYP17) and the steroid 5alpha-reductase type II gene (SRD5A2), two genes that are involved in the biosynthesis and metabolism of androgens in men. The CYP17 MspA1 I polymorphism has been associated with increased prostate cancer risk, and the SRD5A2 V89L polymorphism has been associated with low A-diol-g in Asian men, a serum marker of 5alpha-reductase activity. The purpose of this study was to investigate the association between these two polymorphisms and serum sex hormone concentrations in 621 British men. In particular, we wanted to test the hypotheses that the A2 allele in the CYP17 gene is associated with increased serum testosterone concentrations, and the L allele in the SRD5A2 gene is associated with reduced A-diol-g concentrations. Mean
Complete information for SRD5A2 gene (Protein Coding), Steroid 5 Alpha-Reductase 2, including: function, proteins, disorders, pathways, orthologs, and expression. GeneCards - The Human Gene Compendium
Complete information for SRD5A1 gene (Protein Coding), Steroid 5 Alpha-Reductase 1, including: function, proteins, disorders, pathways, orthologs, and expression. GeneCards - The Human Gene Compendium
Treating symptoms of benign prostatic hyperplasia (BPH) in men who have an enlarged prostate gland. Dutasteride/tamsulosin is a 5 alpha-reductase inhibitor and alpha-blocker combination. The 5 alpha-reductase inhibitor (dutasteride) works by lowering levels of a hormone called dihydrotestosterone (DHT), which is a major cause of prostate growth. The alpha-blocker (tamsulosin) works by relaxing muscles in the prostate and bladder. Dutasteride/tamsulosin helps to decrease the size of the prostate and reduce symptoms of BPH.. Genérico Jalyn (Dutasteride + Tamsulosin 0.5mg + 0.4mg) € 3.03 comprimido -Salud Masculina @ Mydiscountpills.com: Fildena|Cenforce|Vidalista|Tadalista-UPD:2020. Cheap price on popular Indian brand names such as: Fildena, Cenforce, Vidalista, Tadalista and more! Full satisfaction of all Your desires :)
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Dutasteride belongs to a class of drugs called 5-alpha-reductase inhibitors, which block the action of the 5-alpha-reductase enzymes that convert testosterone into dihydrotestosterone (DHT). Finasteride also belongs to this group, but while dutasteride inhibits both isoforms of 5-alpha reductase, finasteride inhibits only one. Even so, a clinical study done by GlaxoSmithKline, the EPICS trial, did not find dutasteride to be more effective than finasteride in treating BPH. [Wikipedia]
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5-Alpha-reductase deficiency is an autosomal recessive intersex condition affecting XY individuals who are born with male gonads, including testicles and Wolffian structures, sometimes with obvious undervirilisation, but usually appear to have female primary sex characteristics.
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Dutasteride, along with Finasteride is a 5-alpha-Reductase inhibitor which are a group of drugs with anti-androgenic properties which inhibit the conversion of testosterone into dihydrotestosterone (DHT). This is the same chemical found in Proscar...
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Finasteride is an FDA-approved hair loss drug that works by blocking an enzyme that would otherwise change testosterone to DHT. It has to be taken every day and may take at least three months to take effect. It can have some side effects, including sexual problems, and its worth noting that if a man stops taking finasteride, the hair he grew back will probably be lost.. Finasteride comes as a tablet to take by mouth. It is usually taken once a day with or without food. Take finasteride at around the same time every day. Follow the directions on your prescription label carefully, and ask your doctor or pharmacist to explain any part you do not understand. Take finasteride exactly as directed. Do not take more or less of it or take it more often than prescribed by your doctor.. If you are taking finasteride to treat BPH, you should know that finasteride may control your condition, but will not cure it. It may take at least 6 months before your symptoms improve. Continue to take finasteride even ...
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3-oxo-5 beta-steroid delta 4-dehydrogenase: do not confuse with EC 1.3.1.23 (cholestenone 5 beta-reductase) which is also steroid 5 beta-reductase in Chemline; do not use for enzyme using NAD(P)-see EC 1.3.1.23 & EC 1.3.1.3
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I have SOS v998 and AE v74. I emailed him today after being reminded of it due to this thread. There is a new SOS due out soon, and there is a fair bit to be added to AE as well, but that one wont be for a while.. The DHT cycling for PE is a good theory, but we have lots of good theories that dont stand up when tested for one reason or another. I believe he got the effects he claimed, but I for one can say that not everyone reacts the same in this instance. I didnt add DHT at the time, because I was unaware of this protocol and was cycling off for other reasons (a rest from it).. I know of no link that shows normal or abnormal levels of DHT being the cause of hairloss. Imho (though plenty will disagree), linking hairloss to DHT is as tenuous a link as excess calories is to obesity; there is certainly a correlation, but it isnt absolutely true either. Hairloss is (as far as we know), an immune response in genetically susceptible follicles rather than a DHT level issue. Thats why Fin, Dut, ...
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Absorption: Following administration of a single 0.5 mg dose of a soft gelatin capsule, time to peak serum concentrations (T max) of dutasteride occurs within 2 to 3 hours. Absolute bioavailability in 5 healthy subjects is approximately 60% (range: 40% to 94%). When the drug is administered with food, the maximum serum concentrations were reduced by 10% to 15%. This reduction is of no clinical significance. Distribution: Pharmacokinetic data following single and repeat oral doses show that dutasteride has a large volume of distribution (300 to 500 L). Dutasteride is highly bound to plasma albumin (99%) and alpha-1 acid glycoprotein (96.6%). In a trial of healthy subjects (n = 26) receiving dutasteride 0.5 mg/day for 12 months, semen dutasteride concentrations averaged 3.4 ng/mL (range, 0.4 to 14 ng/mL) at 12 months and, similar to serum, achieved steady-state concentrations at 6 months. On average, at 12 months 11.5% of serum dutasteride concentrations partitioned into semen.. Metabolism and ...
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Sandoz Dutasteride: Dutasteride belongs to a class of medications known as 5-alpha-reductase inhibitors. It is used to relieve symptoms of benign prostatic hyperplasia (BPH) in men with enlarged prostates. BPH is a noncancerous enlargement of the prostate gland that usually occurs in men after the age of 50.
Dutasteride belongs to a class of drugs called 5α-reductase inhibitors, which block the action of the 5α-reductase enzymes that convert testosterone into DHT.[36] It inhibits all three forms of 5α-reductase, and can decrease DHT levels in the blood by up to 98%.[1][37][38] Specifically it is a competitive, mechanism-based (irreversible) inhibitor of all three isoforms of 5α-reductase, types I, II, and III (IC50 values are 3.9 nM for type I and 1.8 nM for type II).[1][37][39][40] This is in contrast to finasteride, which is similarly an irreversible inhibitor of 5α-reductase[40][41] but only inhibits the type II and III isoenzymes.[37] As a result of this difference, dutasteride is able to achieve a reduction in circulating DHT levels of up to 98%, whereas finasteride is able to achieve a reduction of only 65 to 70%.[38][2][36][42] In spite of the differential reduction in circulating DHT levels, the two drugs decrease levels of DHT to a similar extent of approximately 85 to 90% in the ...
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Is there anyone who uses dutasteride and finasteride together to treat hair loss? Would it increase the chances of growing hair? Or will one eliminate the other? Theres no need or reason to use finasteride (Propecia) and dutasteride (Avodart) together. Finasteride blocks type II 5-alpha-reductase and dutasteride blocks type I and type II. Its 5-alpha-reductase […]. More. ...
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This study is being done to determine how much certain hormone levels in the prostate decrease when a patient takes dutasteride 0.5mg daily for 3 months prior to TURP. Male patients at least 50 years old willing to take either dutasteride or a placebo (dummy pill) once daily by mouth for 3 months prior to having a surgery to reduce the size of their prostate. During the surgery, very small pieces of the prostate that are removed will be tested to see how much dihydrotestosterone and testosterone (male hormones) are in the tissue ...
An orally active testosterone 5-alpha-reductase inhibitor. It is used as a surgical alternative for treatment of benign prostatic hyperplasia. [PubChem]
Androgens are involved in prostate cancer (PCa) cell growth. Genes involved in androgen metabolism mediate key steps in sex steroid metabolism.
According to an article published by CBS News, men with male pattern baldness may have a higher risk of developing aggressive prostate cancer. A study published in the Journal of Clinical Oncology shows that the baldness develops after cumulative, lifelong exposure to cutaneous testosterone. While the testosterone in the skin is not necessarily...
When you lose your hair, the way you perceive yourself can change drastically. In addition it can also change the way others react to you in different aspects of your life. Because of this some people experience male pattern baldness depression. This article explores a number of different ways of treating MPB depression.
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All medicines may cause side effects, but many people have no, or minor, side effects.. Check with your doctor if any of these most common side effects persist or become bothersome:. Back pain; blurred vision; cough; decreased sexual ability; diarrhea; dizziness; drowsiness; lightheadedness; runny or stuffy nose; sinus inflammation; trouble sleeping; weakness.. Seek medical attention right away if any of these severe side effects occur:. Severe allergic reactions (rash; hives; itching; difficulty breathing; tightness in the chest; swelling of the mouth, face, lips, or tongue); chest pain; fainting; fever, chills, or persistent sore throat; irregular heartbeat; prolonged, painful erection; severe of persistent dizziness ...
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Most men value their hair for two main reasons: It makes them younger and it accentuates the face. But as valuable as your hair is the chances ar
Why does baldness affect many men, particularly in later years? Natural hair loss can sometimes cause distress, but it can be partly treated.
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In April, the Food and Drug Administration (FDA) updated the warning to finasteride, Merck & Co.s drug marketed to treat both male pattern baldness (Propecia) and enlarged prostate (Proscar).
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Dutasteride can also be prescribed to treat male pattern hair loss although the FDA has not given specific approval that dutasteride can treat male pattern hair loss. When a medication is prescribed for something else than the FDA has allowed for a companys marketing claims, this is known as off-label.. The manufacturer, GlaxoSmithKline, completed a Phase I and II study of dutasteride for hair loss, but suddenly and unexpectedly, called off the trials in 2002 and no one really knows why. However, these trials were restarted in Korea in 2006 and were completed in January of 2009. The results of this study have not been released yet. However, some early speculation is that it does offer a superior hair count in comparison to finasteride. (2,3,). The promise and hope behind dutasteride over finasteride is that it blocks or inhibits BOTH isoforms of 5-alpha reductase, while finasteride only works on one.. Whether or not dutasteride is clinically proven to be more effective than finasteride, remains ...
Researchers from the Perelman School of Medicine at the University of Pennsylvania have identified an abnormal amount a protein called Prostaglandin D2 in the bald scalp of men with male pattern baldness, a discovery that may lead directly to new treatments for the most common cause of hair loss in men. In both human and animal models, researchers found that a prostaglandin known as PGD2 and its derivative, 15-dPGJ2, inhibit hair growth. The PGD2-related inhibition occurred through a receptor called GPR44, which is a promising therapeutic target for androgenetic alopecia in both men and women with hair loss and thinning.. Male pattern baldness strikes 8 of 10 men under 70 years old, and causes hair follicles to shrink and produce microscopic hairs, which grow for a shorter duration of time than normal follicles.. Researchers took an unbiased approach when scanning for potential biological causes of baldness, looking in scalp tissue from balding and non-bald spots from men with male pattern ...
... ! Dutasteride is used alone or with another medication to treat benign prostatic hyperplasia (BPH; enlargement of the prostate gland). Dutasteride is in a class of medications called 5-alpha reductase inhibitors.
Dutasteride prevents the conversion of testosterone to dihydrotestosterone (DHT) in the body. DHT is involved in the development of benign prostatic hyperplasia (BPH). Dutasteride is used to treat benign prostatic hyperplasia (BPH) in men with an enlarged prostate. Dutasteride helps improve urinary flow and may also...
Dr. Marc Garnick discusses prostate cancer chemoprevention with the use of the 5 Alpha Reductase inhibitors finasteride and dutasteride.
The four-year REDUCE (REduction by DUtasteride of prostate Cancer Events) clinical study evaluated prostate cancer risk reduction in men taking dutasteride, a 5-alpha-reductase inhibitor (5ARI) typically used to treat enlarged prostate. REDUCE results showed that dutasteride decreased the risk of biopsy detectable prostate cancer by 22.8 percent compared to a placebo group, but concerns remained about the drugseffectiveness.
... is used to treat benign prostatic hyperplasia (BPH) in men with an enlarged prostate. Dutasteride helps improve urinary flow and may also reduce your need for prostate surgery later on. This medicine is for use in men only. Dutasteride may also be used for purposes not listed in this medication guide.
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CO Finasteride: Finasteride belongs to a group of medications known as 5-alpha-reductase inhibitors. Finasteride is used to treat benign prostatic hyperplasia (BPH), also known as enlarged prostate. Finasteride can be used alone or in combination with another medication called doxazosin (an alpha blocker). These medications may be taken together to reduce the progress of your BPH symptoms. If you are taking this combination, be sure to also read the patient information for doxazosin.
Balding in men with a typical pattern is commonly known as male pattern baldness. It is also known as androgenic alopecia because it is related to androgen hormones.
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Male pattern balding is a common androgen-dependent trait. The frequency of balding in the population increases with age but not all men develop balding even in old age. It is well-known that balding tends to run in families but the nature of the underlying genetic predisposition and the mode of inheritance are unknown. In this study we examined scalp hair status across a wide age range in 572 men and took family histories of balding in first degree male relatives. The results confirmed that there is an increased frequency of balding in the fathers of young bald men and a high relative risk of balding in young subjects with a balding father but these effects declined with increasing subject age. In contrast, there was a pronounced increase in the frequency of non-balding in the fathers of non-bald elderly subjects and an increased relative risk of non-balding in elderly subjects with a non-bald father, which were not evident in younger subjects. Analysis of the frequencies of balding and ...
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In enzymology, a cholestenone 5alpha-reductase (EC 1.3.1.22) is an enzyme that catalyzes the chemical reaction 5alpha-cholestan ... Other names in common use include testosterone Delta4-5alpha-reductase, steroid 5alpha-reductase, 3-oxosteroid Delta4- ... 4-ene-5alpha-reductase, Delta4-3-ketosteroid 5alpha-oxidoreductase, cholest-4-en-3-one 5alpha-reductase, and testosterone ... 3-oxosteroid 5alpha-reductase, testosterone Delta4-hydrogenase, 4-ene-3-oxosteroid 5alpha-reductase, reduced nicotinamide ...
... alpha -substrate}+NADP+}}} 5α-DHP is a major hormone in circulation of normal cycling and pregnant women. 5α-Reductase is most ... Cholestenone5α-Cholestanone Progesterone → 5α-Dihydroprogesterone 3α-Dihydroprogesterone → Allopregnanolone 3β- ... Killian J, Pratis K, Clifton RJ, Stanton PG, Robertson DM, O'Donnell L (May 2003). "5alpha-reductase isoenzymes 1 and 2 in the ... Thiele S, Hoppe U, Holterhus PM, Hiort O (June 2005). "Isoenzyme type 1 of 5alpha-reductase is abundantly transcribed in normal ...
... cholestenone 5alpha-reductase MeSH D08.811.682.660.250 --- coproporphyrinogen oxidase MeSH D08.811.682.660.275 --- ... gtp-binding protein alpha subunit, gi2 MeSH D08.811.277.040.330.300.200.100.300 --- gtp-binding protein alpha subunits, gq-g11 ... gmp reductase MeSH D08.811.682.655.500 --- nitrate reductases MeSH D08.811.682.655.500.124 --- nitrate reductase MeSH D08.811. ... gtp-binding protein alpha subunits, g12-g13 MeSH D08.811.277.040.330.300.200.100.200 --- gtp-binding protein alpha subunits, gi ...
7-dehydrocholesterol reductase EC 1.3.1.22: cholestenone 5a-reductase EC 1.3.1.23: cholestenone 5b-reductase is identical to EC ... alpha-pinene monooxygenase EC 1.14.13.156: 1,8-cineole 2-endo-monooxygenase EC 1.14.13.157: 1,8-cineole 2-exo-monooxygenase EC ... flavin reductase (NADH) EC 1.5.1.37: FAD reductase (NADH) EC 1.5.1.38: FMN reductase (NADPH) EC 1.5.1.39: FMN reductase (NAD(P) ... zeatin reductase EC 1.3.1.70: D14-sterol reductase EC 1.3.1.71: D24(241)-sterol reductase EC 1.3.1.72: D24-sterol reductase EC ...
In enzymology, a cholestenone 5alpha-reductase (EC 1.3.1.22) is an enzyme that catalyzes the chemical reaction 5alpha-cholestan ... Other names in common use include testosterone Delta4-5alpha-reductase, steroid 5alpha-reductase, 3-oxosteroid Delta4- ... 4-ene-5alpha-reductase, Delta4-3-ketosteroid 5alpha-oxidoreductase, cholest-4-en-3-one 5alpha-reductase, and testosterone ... 3-oxosteroid 5alpha-reductase, testosterone Delta4-hydrogenase, 4-ene-3-oxosteroid 5alpha-reductase, reduced nicotinamide ...
... into 5-alpha-dihydrotestosterone (DHT) and progesterone or corticosterone into their corresponding 5-alpha-3-oxosteroids. It ... cholestenone 5-alpha-reductase activity Source: UniProtKB-EC. *oxidoreductase activity Source: GO_Central ,p>Inferred from ... "Identification of missense mutations in the SRD5A2 gene from patients with steroid 5alpha-reductase 2 deficiency.". Vilchis F. ... "New mutations, hotspots, and founder effects in Brazilian patients with steroid 5alpha-reductase deficiency type 2.". Hackel C. ...
cholestenone 5alpha-reductase;. testosterone Delta4-5alpha-reductase;. steroid 5alpha-reductase;. 3-oxosteroid Delta4- ... 4-ene-5alpha-reductase;. Delta4-3-ketosteroid 5alpha-oxidoreductase;. cholest-4-en-3-one 5alpha-reductase;. testosterone 5alpha ... 5alpha-reductase;. steroid 5alpha-hydrogenase;. 3-oxosteroid 5alpha-reductase;. testosterone Delta4-hydrogenase;. 4-ene-3- ... 5alpha-Reductase activity in Lycopersicon esculentum: cloning and functional characterization of LeDET2 and evidence of the ...
... on phospholipase and on aldose reductase and being useful for the prevention and/or treatment of diseases induced by ... phospholipase and aldose reductase in mammals, especially in human beings. ... R 5 , R 6 , R 7 , R 8 , U, n, m, p, q, R 5 , and R 6 are defined as in the above specification, possessing antagonistic ... activity on leukotrienes (SRS), inhibitory activity on 5α-reductase, ...
Steroid 5 Alpha-Reductase 2, including: function, proteins, disorders, pathways, orthologs, and expression. GeneCards - The ... Micropenis and the 5alpha-reductase-2 (SRD5A2) gene: mutation and V89L polymorphism analysis in 81 Japanese patients. (PMID: ... acting on the CH-CH group of donors and cholestenone 5-alpha-reductase activity. An important paralog of this gene is SRD5A1. ... Alpha Polypeptide 2 (3-Oxo-5 Alpha-Steroid Delta 4-Dehydrogenase Alpha 2) 2 3 ...
Such compounds are useful as selective antagonists of testosterone 5α-reductase 1. ... NHR 5 , and R 5 is selected from the group consisting of hydrogen and C 1-10 alkylcarbonyl. ... 108010066551 Cholestenone 5 alpha-Reductase Proteins 0 description 10 * 229910017917 NH4 Cl Inorganic materials 0 description ... 238000003818 flash chromatography Methods 0 description 5 * 238000004128 high performance liquid chromatography Methods 0 ...
Steroid 5 Alpha-Reductase 2, including: function, proteins, disorders, pathways, orthologs, and expression. GeneCards - The ... alpha}-reductase Type 2 (SRD5a2) gene polymorphisms and risk of prostate cancer: a HuGE review. (PMID: 19914946) Li J … Khoury ... GO annotations related to this gene include oxidoreductase activity, acting on the CH-CH group of donors and cholestenone 5- ... The GeneCards human gene database index: 2 3 5 A B C D E F G H I J K L M N O P Q R S T U V W X Y Z ...
Mechanism of Action Alpha 1 adrenergic receptor antagonists; Cholestenone 5-alpha reductase inhibitors ...
Tumor Necrosis Factor-alpha 腫瘍壊死因子アルファ Fluorenes フルオレン ... Cholestenone 5 alpha-Reductase コレステノン5アルファ-レダクターゼ Sucrase スクラーゼ ... Cortisone Reductase コルチゾンレダクターゼ Enzyme Inhibitors 酵素阻害剤 ... 3-Oxo-5-alpha-Steroid 4-Dehydrogenase 3-ケト-5-アルファ-ステロイドデルタ-
Pyne, N. J. & Pyne, S., 1993, In : Cellular Signalling. 5, 4, p. 401-409 9 p.. Research output: Contribution to journal › ... Inglis, W. L., Dunbar, J. S. & Winn, P., 25 Jun 1993, In : Neuroscience Letters. 156, 1-2, p. 78-82 5 p.. Research output: ... Stack, M. & Stott, F. H., 1993, In : Corrosion Science. 35, 5-8, p. 1027-1034 8 p.. Research output: Contribution to journal › ... Price, C. J., 1 Mar 1993, In : Journal of Crystal Growth. 128, 1-4, p. 1277-1281 5 p.. Research output: Contribution to journal ...
Cholestenone 5 alpha-Reductase Contraceptive Agents, Male Dihydrotestosterone Enzyme Inhibitors Epididymis Female Fertilization ... alpha- steroid 4- dehydrogenase (2). *5 alpha reductase inhibitors (2) ... Actions of 5alpha-reductase inhibitors on the epididymis. Molecular and cellular endocrinology. 2006 May 16;250(1-2):190-5 ... Two isozymes of 5alpha-reductase, types 1 and 2, are abundantly expressed in the epididymis. DHT is the androgen found in the ...
Simmons, J. D., Dearmond, D. T. & Calhoon, J. H., Jan 5 2012, Cardiothoracic Surgery Review. Wolters Kluwer Health Adis (ESP), ... 5. p. 291-327 37 p.. Research output: Chapter in Book/Report/Conference proceeding › Chapter ... Conway, D. L., May 5 2011, Stillbirth: Prediction, Prevention and Management. Wiley-Blackwell, p. 117-131 15 p.. Research ... Saltzman, W., Tardif, S. D. & Rutherford, J. N., Dec 1 2011, Hormones and Reproduction of Vertebrates - Volume 5. Elsevier Inc. ...
The type 1 5alpha-reductase selective inhibitor 4,7beta-dimethyl-4-aza-5alpha-cholestan-3-one, but not the type 2 selective ... Cholestenone 5 alpha-Reductase. *Cyproterone Acetate/pharmacology. *Dehydroepiandrosterone/metabolism. *Enzyme Inhibitors/ ... Furthermore, the effects of the selective 5alpha-reductase type 1 and 2 inhibitors, 4,7beta-dimethyl-4-aza-5alpha-cholestan-3- ... Type 2 17beta-hydroxysteroid dehydrogenase, type 1 5alpha-reductase, and 3alpha-hydroxysteroid dehydrogenase mRNA were ...
... cholestenone 5-alpha-reductase activity • amide binding • NADPH binding... ... cholestenone 5-alpha-reductase activity. • amide binding. • NADPH binding. • electron carrier activity. • oxidoreductase ... 3-oxo-5-alpha-steroid 4-dehydrogenase activity. Cellular component. • cytoplasm. • integral component of membrane. • organelle ...
Adrenergic alpha-Antagonists/therapeutic use , Cholestenone 5 alpha-Reductase/antagonists & inhibitors , Data Collection , ... Effect of selective 5alpha-reductase inhibitor or/and testosterone undecanoate on the reproductive function of male rats / 中华男科 ... Humans , Male , Adrenergic alpha-Antagonists , Cholestenone 5 alpha-Reductase/antagonists & inhibitors , Phytotherapy , ... Of the respondents, 57.2% had prescribed alpha blocker and 41.6% alpha blocker plus 5-alpha reductase inhibitors as the medical ...
Adrenergic alpha-Antagonists/therapeutic use , Cholestenone 5 alpha-Reductase/antagonists & inhibitors , Data Collection , ... Humans , Male , Adrenergic alpha-Antagonists , Cholestenone 5 alpha-Reductase/antagonists & inhibitors , Phytotherapy , ... Of the respondents, 57.2% had prescribed alpha blocker and 41.6% alpha blocker plus 5-alpha reductase inhibitors as the medical ... The prescription of 5-ARIs was dependent on the size of the prostate and the severity of symptoms. CONCLUSION: The results of ...
... is an orally-active 5α-reductase inhibitor developed by Ono (Japan) for the treatment of benign prostatic hyperplasia. It ... Mechanism of Action Cholestenone 5-alpha reductase inhibitors * Orphan Drug Status Orphan designation is assigned by a ...
PubMed journal article Lifestyle determinants of 5alpha-reductase metabolites in older African-American, white, and Asian- ... 17-diolAndrosteroneAsian Continental Ancestry GroupBiomarkersBritish ColumbiaCaliforniaCase-Control StudiesCholestenone 5 alpha ... Lifestyle determinants of 5alpha-reductase metabolites in older African-American, white, and Asian-American men.. Cancer ... "Lifestyle Determinants of 5alpha-reductase Metabolites in Older African-American, White, and Asian-American Men." Cancer ...
Adrenergic alpha-Antagonists/therapeutic use , Cholestenone 5 alpha-Reductase/antagonists & inhibitors , Data Collection , ... Of the respondents, 57.2% had prescribed alpha blocker and 41.6% alpha blocker plus 5-alpha reductase inhibitors as the medical ... Adrenergic alpha-Antagonists / Cholestenone 5 alpha-Reductase / Korea Clinical aspect: Diagnosis / Therapy Country/Region as ... The prescription of 5-ARIs was dependent on the size of the prostate and the severity of symptoms. CONCLUSION:. The results of ...
... alpha -substrate}+NADP+}}} 5α-DHP is a major hormone in circulation of normal cycling and pregnant women. 5α-Reductase is most ... Cholestenone5α-Cholestanone Progesterone → 5α-Dihydroprogesterone 3α-Dihydroprogesterone → Allopregnanolone 3β- ... Killian J, Pratis K, Clifton RJ, Stanton PG, Robertson DM, ODonnell L (May 2003). "5alpha-reductase isoenzymes 1 and 2 in the ... Thiele S, Hoppe U, Holterhus PM, Hiort O (June 2005). "Isoenzyme type 1 of 5alpha-reductase is abundantly transcribed in normal ...
Aged , Bias , Cholestenone 5 alpha-Reductase , Follow-Up Studies , Freedom , Humans , Male , Mass Screening , Prostate-Specific ... Cholestenone 5 alpha-Reductase / Freedom Type of study: Screening_studies Clinical aspect: Diagnosis / Prognosis Language: ... and those with a history of medication with 5 alpha-reductase inhibitors. Serum PSA underwent logarithmic conversion to work ...
Cholestenone 5alpha-reductase Current Synonym true false 2647400010 3-Oxo-5alpha-steroid delta^4^-dehydrogenase Current Synonym ... Testosterone 5-alpha-reductase Current Synonym true false 144134010 ... Cholestenone 5alpha-reductase (substance). Code System Preferred Concept Name. Cholestenone 5alpha-reductase (substance). ...
... est le premier et le.Cholestenone 5 alpha-Reductase. as well as 5 alpha-reductase inhibitors N,N-diethyl-4-methyl-3-oxo-4-aza-5 ... My online accutane order behinds whenever im decreasing low,. In addition, alpha-methyl-p-tyrosine,. Hmg coa-reductase ... Crestor is a HMG CoA reductase {inhibitor,prevention} {used.. Defect in dihydropteridine reductase - Orphanet. Free online ... Ribonucleotide reductase inhibitor : définition de. Generic Avodart (Dutas) is a. dutasteride belongs to a group of 5-alpha- ...
The effects of synthetic alpha-subunit peptides on thyroid-stimulating immunoglobulin activity.. 1988 J C 3rd Morris et al. ... Aged, Aged, 80 and over, Cholestenone 5 alpha-Reductase, Dihydrotestosterone, metabolism, Epithelium, enzymology, Humans, ... Cyclic AMP, biosynthesis, Female, Glycoprotein Hormones, alpha Subunit, Graves Disease, immunology, Humans, Immunoglobulin G, ... Kinetic parameters of 5 alpha-reductase activity in stroma and epithelium of normal, hyperplastic, and carcinomatous human ...
A 70-80% blocking of the 5a reductase wont go stopping its other functions which in the first place are meagre, secondly I ... Cholestenone5α-Cholestanone. *Progesterone → 5α-Dihydroprogesterone. *3α-Dihydroprogesterone → Allopregnanolone ... Testosterone → 5α-Dihydrotestosterone. To prove the safety of finasteride, you need to show that every single one of those ... Just a side note, finasteride doesnt target DHT, it targets 5-alpha reductase and thus affects a large number of hormones in ...
  • The reaction involves a stereospecific and permanent break of the Δ4,5 with the help of NADPH as a cofactor. (wikipedia.org)
  • 5α-R2 is expressed in prostate, seminal vesicles, epididymis, liver, and to a lesser extent the scalp and skin. (wikipedia.org)
  • Restriction analysis of cDNA fragments was performed to identify isozymes of 3beta-hydroxysteroid dehydrogenase/Delta(5-4)-isomerase and 3alpha-hydroxysteroid dehydrogenase. (nih.gov)
  • Androgen receptor mRNA was detected in SZ95 sebocytes and HaCaT keratinocytes but not in MeWo melanoma cells, whereas 3beta-hydroxysteroid dehydrogenase/Delta(5-4)-isomerase isotype 1 mRNA and metabolic activity were only found in SZ95 sebocytes. (nih.gov)
  • LUTS and ED were assessed using the International Prostate Symptom Score (IPSS) and International Index of Erectile Function-5 (IIEF-5), respectively. (bvsalud.org)
  • The five-item version of the International Index of Erectile Function (IIEF-5), International Prostate Symptom Score (IPSS), Qmax, and residual urine volume(PVR) were assessed immediately before initiation of treatment (V1) and after four (V2) and twelve weeks of treatment (V3). (bvsalud.org)
  • RESULTS: No difference of IIEF-5, IPSS, Qmax, and PVR between two groups in V1. (bvsalud.org)
  • 5α-dihydroaldosterone is a potent antinatriuretic agent, although different from aldosterone. (wikipedia.org)
  • 5α-R1 and 5α-R2 appear to be expressed in the prostate in male fetuses and throughout postnatal life. (wikipedia.org)
  • The prescription of 5-ARIs was dependent on the size of the prostate and the severity of symptoms. (bvsalud.org)
  • In socially isolated mice, 5α-R1 is specifically down-regulated in glutamatergic pyramidal neurons that converge on the amygdala from cortical and hippocampal regions. (wikipedia.org)
  • All the mice except those in the blank control group were subcutaneously injected with testosterone propionate (5 mg / [kg·d]) at 7 days after surgical castration. (bvsalud.org)
  • Methods: Thirty mice were randomized into 5 groups (G) of 6 animals each. (bvsalud.org)
  • 5α-R1 is expressed in fetal scalp and nongenital skin of the back, anywhere from 5 to 50 times less than in the adult. (wikipedia.org)
  • 5α-R2 is expressed in fetal prostates similar to adults. (wikipedia.org)
  • The HRV parameters were evaluated while patients remained seated for 5 minutes, and frequency and time domain analyses were then performed. (bvsalud.org)
  • Regarding the initial drugs prescribed, the use of alpha-blockers was common in both groups. (bvsalud.org)
  • During 4 weeks of healing, 1 hour of HBO therapy was applied to the rats in the HBO groups 5 times a week. (bvsalud.org)
  • RESULTS: The mean patient age was 69.1 years (range, 50-85 years), the mean parity was 2.79 times (range, 2-5 times), and the mean follow-up period was 45.6 months (range, 21-72 months). (bvsalud.org)
  • Four subjects (0.6%) reported 5 SAEs (right radius fracture, 2 events of chronic follicular tonsillitis, influenza infection, and acute appendicitis). (bvsalud.org)
  • The median follow-up period was 75.5 months (range, 5 to 195 months). (bvsalud.org)
  • The HA phylogenetic tree revealed that 87.5% (7/8) of BV strains coexisted with the vaccine strain in one branch, while 88.98% (8/9) of BY strains from 2013 to 2015 were not in the same branch as the corresponding vaccine strain, with 5 epitope site mutions N116K, S150L, N165Y, D196N and N202S. (bvsalud.org)