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 1.1.1.62Secosteroids: Steroids in which fission of one or more ring structures and concomitant addition of a hydrogen atom at each terminal group has occurred.Estradiol: The 17-beta-isomer of estradiol, an aromatized C18 steroid with hydroxyl group at 3-beta- and 17-beta-position. Estradiol-17-beta is the most potent form of mammalian estrogenic steroids.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.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.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.Receptors, Estradiol: Cytoplasmic proteins that bind estradiol, migrate to the nucleus, and regulate DNA transcription.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.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).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.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 1.1.1.14
Thus, the two substrates of this enzyme are cholest-5-ene-3β,7α-diol and NAD+, whereas its 3 products are 7α-hydroxycholest-4-en-3-one, NADH, and H+. The systematic name of this enzyme class is cholest-5-ene-3β,7α-diol:NAD+ 3-oxidoreductase. This enzyme is also called 3β-hydroxy-Δ5-C27-steroid oxidoreductase. The human version of this enzyme is known as hydroxy-Δ-5-steroid dehydrogenase, 3 β- and steroid delta-isomerase 7 or HSD3B7 which is encoded by the HSD3B7 gene.[2][3] ...
Term a ddefnyddir o fewn mathemateg a gwyddor cyfrifiadur yw algorithm. Mae'n diffinio set o weithrediadau i'w perfformio un cam ar y tro. Gall algorithmau berfformio tasgau cyfrif, prosesu data, ac/neu dasgau rhesymu awtomatig. Gellir defnyddio'r term yn anffurfiol i ddisgrifio pob rhaglen gyfrifiadurol, ond yn dechnegol, dylid defnyddio 'algorithm' ond i ddisgrifio rhaglen y bydd yn sicr, yn y diwedd, o ddod i derfyn y dasg.[1] ...
... , sold under the brand names Femtrace, Femring, and Menoring, is an estrogen medication which is used in hormone therapy for the treatment of menopausal symptoms in women.[3][4][5][6] It is taken by mouth or given as a vaginal ring once every three months.[1] Side effects of estradiol acetate include breast tenderness, breast enlargement, nausea, headache, and fluid retention.[7][5][6] Estradiol acetate is a synthetic estrogen and hence is an agonist of the estrogen receptor (ER), the biological target of estrogens like estradiol.[8][9] It is an estrogen ester and a prodrug of estradiol in the body.[9][8] Because of this, it is considered to be a natural and bioidentical form of estrogen.[9] Estradiol acetate was introduced for medical use in 2001.[10] It is available in the United States and the United Kingdom.[10][3] The formulation for use by mouth has been discontinued in the United States.[11] .mw-parser-output ...
The classical estrogen receptors first characterized in 1958[6] are water-soluble proteins located in the interior of cells that are activated by estrogenenic hormones such as estradiol and several of its metabolites such as estrone or estriol. These proteins belong to the nuclear hormone receptor class of transcription factors that regulate gene transcription. Since it takes time for genes to be transcribed into RNA and translated into protein, the effects of estrogens binding to these classical estrogen receptors is delayed. However, estrogens are also known to have effects that are too fast to be caused by regulation of gene transcription.[7] In 2005, it was discovered that a member of the G protein-coupled receptor (GPCR) family, GPR30 also binds with high affinity to estradiol and is responsible in part for the rapid non-genomic actions of estradiol. Based on its ability to bind estradiol, GPR30 was renamed as G protein-coupled estrogen ...
Levels of estradiol in premenopausal women are highly variable throughout the menstrual cycle and reference ranges widely vary from source to source.[60] Estradiol levels are minimal and according to most laboratories range from 20 to 80 pg/mL during the early to mid follicular phase (or the first week of the menstrual cycle, also known as menses).[61][62] Levels of estradiol gradually increase during this time and through the mid to late follicular phase (or the second week of the menstrual cycle) until the pre-ovulatory phase.[60][61] At the time of pre-ovulation (a period of about 24 to 48 hours), estradiol levels briefly surge and reach their highest concentrations of any other time during the menstrual cycle.[60] Circulating levels are typically between 130 and 200 pg/mL at this time, but in some women may be as high as 300 to 400 pg/mL, and the upper limit of the reference range of some laboratories are even greater (for instance, 750 ...
Levels of estradiol in premenopausal women are highly variable throughout the menstrual cycle and reference ranges widely vary from source to source.[59] Estradiol levels are minimal and according to most laboratories range from 20 to 80 pg/mL during the early to mid follicular phase (or the first week of the menstrual cycle, also known as menses).[60][61] Levels of estradiol gradually increase during this time and through the mid to late follicular phase (or the second week of the menstrual cycle) until the pre-ovulatory phase.[59][60] At the time of pre-ovulation (a period of about 24 to 48 hours), estradiol levels briefly surge and reach their highest concentrations of any other time during the menstrual cycle.[59] Circulating levels are typically between 130 and 200 pg/mL at this time, but in some women may be as high as 300 to 400 pg/mL, and the upper limit of the reference range of some laboratories are even greater (for instance, 750 ...
The first CIC to be studied was estradiol valerate/hydroxyprogesterone caproate (EV/OHPC) in 1963, and the second CIC to be studied was estradiol enantate/algestone acetophenide (E2-EN/DHPA) in 1964.[18][17] In 1967, E2-EN/DHPA was in the late stages of clinical development.[25][18] By 1969, the medication was available for medical use under the brand name Perlutal.[26] Within a few years, it was marketed under other brand names such as Topasel and Ova-Repos as well.[27][28][29][30] In addition, several other CICs had been introduced for medical use by 1972.[30] By 1976, two major CICs were in use: E2-EN/DHPA (brand names Perlutan, Topasel) in Spain and Latin America, and EV/OHPC (brand name Injectable No. 1) in China.[31] These CICs have been described as first-generation CICs.[31] Two second-generation CICs, estradiol cypionate/medroxyprogesterone acetate (EC/MPA; brand names Cyclofem and later Lunelle) and estradiol ...
LH supports theca cells in the ovaries that provide androgens and hormonal precursors for estradiol production. At the time of menstruation, FSH initiates follicular growth, specifically affecting granulosa cells.[7] With the rise in estrogens, LH receptors are also expressed on the maturing follicle, which causes it to produce more estradiol. Eventually, when the follicle has fully matured, a spike in 17α-hydroxyprogesterone production by the follicle inhibits the production of estrogens, leading to a decrease in estrogen-mediated negative feedback of GnRH in the hypothalamus, which then stimulates the release of LH from the anterior pituitary.[8] However another theory of the LH peak is a positive feedback mechanism from estradiol. The levels keep rising through the follicular phase and when they reach an unknown threshold, this results in the peak of the LH.[9] This effect is opposite from the usual negative feedback mechanism presented at lower levels. ...
... (-utawa oestrogen) -ya iku sekelompok senyawa steroid kang fungsine mligi minangka hormon seks wanita. Sanajan turah bisa iku ing jero awak priya utawa wanita, kandungane luwih dhuwur ing awak wanita umur subur. Hormon iki nyebapake perkembangan lan nahanake tanda-tanda kelamin sékundhèr ing wanita, kaya susu, lan uga mèlu sajrone kekandelan endometrium utawa sajrone pengaturan siklus haid. nalika wektu menopause, estrogen wiwit kurang saéngga bisa nyebapake pira-pira efek, ing antarané hot flash, kanti kringet nalika wektu turu, lan was-was kang ora wajar. telu jinis estrogen utama kang turah kanthi alami sajrone awak wanita ya iku estradiol, estriol, lan estron. Awit menarche nganti menopause, estrogen utama -ya iku 17β-estradiol. Ing jero awak, katelu jinis estrogen mau digawé saka androgen kanti bantuan enzim. Estradiol digawé saka testosteron, wondene estron digawé saka androstenadion. Estron kanti sipat luwih lemah ketimbang ...
Oestrogen (or estrogen) is a group of female hormones.[1] It includes oestrone (E1), oestradiol (E2), and oestriol (E3). Oestradiol is the most important oestrogen. Oestrogen is mainly secreted by the ovary, a small amount by the liver, adrenal cortex, and breast. In pregnancy, the placenta can also have a lot of secretion. Male testes also secrete a small amount. Ovary mainly secretes β-estradiol, other estrogens are less important.[2] Oestrogen helps women grow during puberty and is part of the menstrual cycle. During menopause, oestrogen levels go down. The male hormone that is similar is androgen. ...
Mueller, G.C. and Rumney, G. (1957). "Formation of 6β-hydroxy and 6-keto derivatives of estradiol-16-C14 by mouse liver microsomes". J. Am. Chem. Soc. 79: 1004-1005. ...
LH djeluje na Leidigove ćelije testisa , što se regulira putem GnRH.[9] Leydigove ćelije proizvode testosteron (T) pod kontrolom LH, koji regulira ekspresiju enzima 17-β hidroksisteroid-dehidrogenaze koji se koristi za pretvaranje androstenediona, hormona koji proizvodi gonada, testosterona,[10] i androgena, koji i endokrinu i intratestikulsku aktivnosti u spermatogenezi. LH se luči iz hipofize, a pod kontrolom impulsa oslobađajućeg hormona gonadotropina (GnRH). Kada su razine T niske, GnRH se oslobađa iz hipotalamusa, stimuliranjem hipofize za oslobađanje LH. [9] Kako se razina T povećava, to će djelovati na hipotalamus i hipofizu preko negativne povratne petlje i inhibiraju oslobađanje GnRH, a posljedično i LH.[10] Androgeni (T, DHT) inhibiraju monoaminooksidaze (MAO) u epifizi, što dovodi do povećanja melatonina i smanjenja LH i FSH putem povećanja GnIH i sekrecije, što izaziva sinteza pod uticajem melatonina. T se može biti aromatiziran u estradiol (E2) da inhibira LH. E2 ...
Steroid je organska spojina s štirimi obroči, razporejenimi v določeno molekularno konfiguracijo. Nekaj primerovː lipidni holesterol, spolna hormona estradiol in testosteron[1] ter protivnetno zdravilo deksametazon.[2] Steroidi imajo dve glavni biološki funkciji: nekateri (npr. holesterol) so pomembne komponente celične membrane, ki spremenijo membransko fluidnost, mnogi steroidi pa so signalne molekule, ki vključijo steroidne receptorje. Steroidni osnovni skelet je sestavljen iz sedemnajstih ogljikovih atomov, povezanih v štiri "kondenzirane" obroče: tri šestčlenske cikloheksanske obroče (obroči A, B in C na prvi sliki) in en petčlenski ciklopentanski obroč (obroč D). Steroidi se med seboj razlikujejo po funkcionalnih skupinah, vezanih na ta štiriobročno jedro, in po oksidacijskem stanju obročev. Steroli so oblika steroidov s hidroksilno skupino na položaju 3 in skeletom, ki izvira iz holestana.[3]:1785f [4] Lahko se razlikujejo tudi bolj izrazito glede na spremembe obročne ...

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