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| Estradiol (E2), also called oestrogen, oestradiol, is an estrogen steroid hormone and the major female sex hormone. It is involved in the regulation of female reproductive cycles such as estrous and menstrual cycles. Estradiol is responsible for the development of female secondary sexual characteristics such as the breasts, widening of the hips and a female pattern of fat distribution. It is also important in the development and maintenance of female reproductive tissues such as the mammary glands, uterus and vagina during puberty, adulthood and pregnancy. It also has important effects in many other tissues including bone, fat, skin, liver, and the brain.
Though estradiol levels in males are much lower than in females, estradiol has important roles in males as well. Apart from humans and other mammals, estradiol is also found in most vertebrates and crustaceans, insects, fish, and other animal species.
Estradiol is produced within the follicles of the ovaries and in other tissues including the testicles, the adrenal glands, fat, liver, the breasts, and the brain. Estradiol is produced in the body from cholesterol through a series of reactions and intermediates. The major pathway involves the formation of androstenedione, which is then converted by aromatase into estrone and is subsequently converted into estradiol. Alternatively, androstenedione can be converted into testosterone, which can then be converted into estradiol. Upon menopause in females, production of estrogens by the ovaries stops and estradiol levels decrease to very low levels.
In addition to its role as a natural hormone, estradiol is used as a medication, for instance in menopausal hormone therapy, and feminizing hormone therapy for transgender women and other genderqueer individuals; for information on estradiol as a medication, see the estradiol (medication) article. |
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Read full article at Wikipedia
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InChI=1S/C18H24O2/c1- 18-9-8-14-13-5-3-12(19)10-11(13)2-4-15(14)16(18)6-7-17(18)20/h3,5,10,14-17,19-20H,2,4,6-9H2,1H3/t14-,15-,16+,17+,18+/m1/s1 |
| VOXZDWNPVJITMN-ZBRFXRBCSA-N |
| [H][C@]12CC[C@]3(C)[C@@H](O)CC[C@@]3([H])[C@]1([H])CCc1cc(O)ccc21 |
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Mus musculus
(NCBI:txid10090)
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Source: BioModels - MODEL1507180067
See:
PubMed
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Daphnia magna
(NCBI:txid35525)
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See:
Changes in the Metabolic Elimination Profile of Testosterone Following Exposure of the Crustacean Daphnia magna to TributyltinGerald A. LeBlanc and James B. McLachlanEcotoxicology and Environmental Safety 45, 296-303 (2000)
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Homo sapiens
(NCBI:txid9606)
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See:
DOI
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estrogen
A hormone that stimulates or controls the development and maintenance of female sex characteristics in mammals by binding to oestrogen receptors. The oestrogens are named for their importance in the oestrous cycle. The oestrogens that occur naturally in the body, notably estrone, estradiol, estriol, and estetrol are steroids. Other compounds with oestrogenic activity are produced by plants (phytoestrogens) and fungi (mycoestrogens); synthetic compounds with oestrogenic activity are known as xenoestrogens.
(via estradiol )
Daphnia magna metabolite
A Daphnia metabolite produced by the species Daphnia magna.
human metabolite
Any mammalian metabolite produced during a metabolic reaction in humans (Homo sapiens).
(via estradiol )
EC 1.2.3.1 (aldehyde oxidase) inhibitor
An EC 1.2.3.* (oxidoreductase acting on donor aldehyde/oxo group with oxygen as acceptor) inhibitor which interferes with the action of aldehyde oxidase (EC 1.2.3.1).
mouse metabolite
Any mammalian metabolite produced during a metabolic reaction in a mouse (Mus musculus).
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geroprotector
Any compound that supports healthy aging, slows the biological aging process, or extends lifespan.
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View more via ChEBI Ontology
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estra-1,3,5(10)-triene-3,17β-diol
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(17β)-estra-1,3,5(10)-triene-3,17-diol
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ChemIDplus
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17beta oestradiol
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ChEBI
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17β-estra-1,3,5(10)-triene-3,17-diol
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NIST Chemistry WebBook
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17β-estradiol
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UniProt
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17β-estradiol
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NIST Chemistry WebBook
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17β-oestradiol
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NIST Chemistry WebBook
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beta-Estradiol
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KEGG COMPOUND
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cis-estradiol
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NIST Chemistry WebBook
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Estradiol
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KEGG COMPOUND
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ESTRADIOL
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PDBeChem
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Estradiol-17beta
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KEGG COMPOUND
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Estradiol-17beta
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KEGG COMPOUND
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1057
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DrugCentral
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5554
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ChemSpider
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C00951
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KEGG COMPOUND
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D00105
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KEGG DRUG
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DB00783
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DrugBank
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EST
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PDBeChem
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Estradiol
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Wikipedia
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HMDB0000151
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HMDB
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LMST02010001
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LIPID MAPS
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LSM-2421
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LINCS
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| View more database links |
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1914275
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Reaxys Registry Number
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Reaxys
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290805
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Gmelin Registry Number
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Gmelin
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50-28-2
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CAS Registry Number
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KEGG COMPOUND
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50-28-2
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CAS Registry Number
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ChemIDplus
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50-28-2
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CAS Registry Number
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NIST Chemistry WebBook
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Ye X, Linton JM, Schork NJ, Buck LB, Petrascheck M (2014)
A pharmacological network for lifespan extension in Caenorhabditis elegans.
Aging cell 13, 206-215 [PubMed:24134630]
[show Abstract]
One goal of aging research is to find drugs that delay the onset of age-associated disease. Studies in invertebrates, particularly Caenorhabditis elegans, have uncovered numerous genes involved in aging, many conserved in mammals. However, which of these encode proteins suitable for drug targeting is unknown. To investigate this question, we screened a library of compounds with known mammalian pharmacology for compounds that increase C. elegans lifespan. We identified 60 compounds that increase longevity in C. elegans, 33 of which also increased resistance to oxidative stress. Many of these compounds are drugs approved for human use. Enhanced resistance to oxidative stress was associated primarily with compounds that target receptors for biogenic amines, such as dopamine or serotonin. A pharmacological network constructed with these data reveal that lifespan extension and increased stress resistance cluster together in a few pharmacological classes, most involved in intercellular signaling. These studies identify compounds that can now be explored for beneficial effects on aging in mammals, as well as tools that can be used to further investigate the mechanisms underlying aging in C. elegans. | Visagie MH, Birkholtz LM, Joubert AM (2014)
17-beta-estradiol analog inhibits cell proliferation by induction of apoptosis in breast cell lines.
Microscopy research and technique 77, 236-242 [PubMed:24449492]
[show Abstract]
Microtubules are important targets when studying potential anticancer agents since disturbance of these microtubule dynamics results in cell cycle arrest and cell death. 2-Methoxyestradiol is a naturally occurring metabolite that exerts antiproliferative activity and induces apoptosis. Due to limited biological accessibly and rapid metabolic degradation, several analogs were synthesized. This study investigated the antiproliferative influence of an 2-methoxyestradiol analog, (8R, 13S, 14S, 17S)-2-Ethyl-13-methyl-7, 8, 9, 11, 12,13, 14, 15, 16, 17-decahydro-6H-cyclopenta[a]phenanthrane-3, 17-diyl bis(sulfamate) (EMBS) on cell proliferation, morphology and apoptosis induction in a estrogen receptor-positive breast adenocarcinoma cells line (MCF-7), estrogen receptor-negative highly metastatic breast cell line (MDA-MB-231) and a non-tumorigenic breast epithelial cell line (MCF-12A). Spectrophotometry results indicated that EMBS exerted differential antiproliferative activity in the three cell lines. Cell growth of the breast adenocarcinoma and highly metastatic breast cell line reached a plateau effect at 0.4 μM after 24 h of exposure. Light microscopy and polarization-optical transmitted light differential interference contrast demonstrated compromised cell density, cells blocked in metaphase and the presence of apoptotic characteristics after EMBS exposure for 24 h in all three cell lines. Transmission electron microscopy and scanning electron microscopy revealed hallmarks of apoptosis namely the presence of apoptotic bodies, shrunken cells and cell debris in EMBS-exposed cells. This investigation demonstrated that EMBS does exert antimitotic activity and induces apoptosis contributing to elucidating the signal transduction of EMBS in tumorigenic and non-tumorigenic breast cell lines. Findings warrant in-depth analysis of specific targets in vitro and subsequent in vivo investigation for anticancer therapy. | Fedotova IuO, Sapronov NS (2013)
[Chronic administration of RJR-2403 in combination with low-dose of 17beta-estradiol corrects passive avoidance learning in ovariectomized rats].
Eksperimental'naia i klinicheskaia farmakologiia 76, 3-6 [PubMed:23901460]
[show Abstract]
The aim of this work was to study the effect of stimulation or blockade of Na7-cholinoreceptors with a low dose of 17beta-estradiol on the passive avoidance performance and behavior in the open-field test in adult ovariectomized (OVX) female rats. Agonist of Na7-cholinoreceptors RJR-2403 (1.0 mg/kg, i.p.) or antagonist of Na7-cholinoreceptors mecamylamine (1.0 mg/kg, i.p.) treated chronically (14 days) alone and in a combination with low dose of 17beta-estradiol (0.5 microg/rat, s.c.) to OVX rats. Co-administration of RJR-2403 with low dose of 17P-estradiol completely restored impaired passive avoidance performance in OVX females. OVX rats treated with RJR-2403 and low dose of 17beta-estradiol demonstrated increased exploratory and grooming behavior in the open-field test. Both mecamylamine alone and in combination with low dose of 17beta-estradiol failed to influence the passive avoidance learning and failed to modify behavior in the open-field test in OVX rats. The results of the present study suggest positive effect of RJR-2403 in combination with low dose of 17beta-estradiol on passive avoidance learning at estrogen deficiency. | Garcia-Segura LM, Sanz A, Mendez P (2006)
Cross-talk between IGF-I and estradiol in the brain: focus on neuroprotection.
Neuroendocrinology 84, 275-279 [PubMed:17124377]
[show Abstract]
The actions of estradiol in the brain involve the interaction with growth factors, such as insulin-like growth factor-I (IGF-I). Many cells in the brain coexpress receptors for estradiol (ERs) and IGF-I (IGF-IR) and both factors interact to regulate neural function. Several studies have shown that there is an interaction of IGF-IR and ERs in neuroprotection. Neuroprotective effects of estradiol are blocked by the inhibition of IGF-IR signaling, while the neuroprotective effects of IGF-I are blocked by the inhibition of ER signaling. These findings suggest that the neuroprotective actions of estradiol and IGF-I after brain injury depend on the coactivation of both ERs and IGF-IR in neural cells. The relationship of ERalpha with IGF-IR through the phosphatidylinositol 3-kinase/Akt/glycogen synthase kinase 3beta (PI3K/Akt/GSK3) signaling pathway may represent the point of convergence used by estradiol and IGF-I to cooperatively promote neuroprotection. Administration of estradiol to ovariectomized rats results in the association of ERalpha with IGF-IR and with components of the PI3K/Akt/GSK3 signaling pathway and in the regulation of the activity of Akt and GSK3 in the brain. Conversely, IGF-I regulates ERalpha transcriptional activity in neuroblastoma cells and the PI3K/Akt/GSK3 signaling pathway is involved in this effect. | Tankó LB, Christiansen C (2005)
Effects of 17beta-oestradiol plus different doses of drospirenone on adipose tissue, adiponectin and atherogenic metabolites in postmenopausal women.
Journal of internal medicine 258, 544-553 [PubMed:16313478]
[show Abstract]
ObjectiveTo investigate how variation in the dose of the progestogen influence the impact of 17beta-oestradiol plus drospirenone (DRSP) treatment on adipose tissue and its secretor function with direct implications for atherogenic metabolites.DesignRandomized, double-blind, placebo-controlled trial.SettingPrimary care, single study site.SubjectsA total of 240 healthy postmenopausal women 53-65 years old, 178 completer.InterventionDaily treatment with 1 mg 17beta-oestradiol plus 1, 2, or 3 mg DRSP, or placebo for 2 years.Main outcome measuresAbsolute changes in central (CFM) and peripheral fat mass (PFM; dual-energy X-ray absorptiometry, DEXA), adipokines [interleukin (IL)-6 and adiponectin], atherogenic metabolites [triglycerides, high-density lipoprotein cholesterol (HDL-C), glucose] and blood pressure.ResultsOestradiol plus 1 mg DRSP evoked significant decreases in CFM and the CFM/PFM ratio from baseline. These benefits virtually decreased with increasing dose of DRSP confounded by dose-dependent increases in CFM and PFM in smokers (P-value for trends <0.001), in whom the increases in bioavailable oestradiol were half of that in nonsmokers (P < 0.001). Treatment with 3 mg DRSP induced decreases in serum adiponectin by month 6 (P < 0.05), which persisted in nonsmokers only and led to significant increases in glucose and triglycerides and decreases in HDL-C (P < 0.05). Adiponectin in smokers normalized by the end of the study parallel with the increases in body fat mass.ConclusionsInteractions of the sex steroids with adipose tissue and its secretor function are important determinants of the overall impact of hormone therapy on cardiovascular risk. A DRSP dose up to 2 mg does not seem to exert adverse effects when combined with 1 mg 17beta-oestradiol. | Obach RS, Huynh P, Allen MC, Beedham C (2004)
Human liver aldehyde oxidase: inhibition by 239 drugs.
Journal of clinical pharmacology 44, 7-19 [PubMed:14681337]
[show Abstract]
The authors tested 239 frequently used drugs and other compounds for their potential to inhibit the drug-metabolizing enzyme, aldehyde oxidase, in human liver cytosol. A sensitive, moderate throughput HPLC-MS assay was developed for 1-phthalazinone, the aldehyde oxidase-catalyzed product of phthalazine oxidation. Inhibition of this activity was examined for the 239 drugs and other compounds of interest at a test concentration of 50 microM. Thirty-six compounds exhibited greater than 80% inhibition and were further examined for measurement of IC50. The most potent inhibitor observed was the selective estrogen receptor modulator, raloxifene (IC50=2.9 nM), and tamoxifen, estradiol, and ethinyl estradiol were also potent inhibitors. Other classes of drugs that demonstrated inhibition of aldehyde oxidase included phenothiazines, tricyclic antidepressants, tricyclic atypical antipsychotic agents, and dihydropyridine calcium channel blockers, along with some other drugs, including loratadine, cyclobenzaprine, amodiaquine, maprotiline, ondansetron, propafenone, domperidone, quinacrine, ketoconazole, verapamil, tacrine, and salmeterol. These findings are discussed in context to potential drug interactions that could be observed between these agents and drugs for which aldehyde oxidase is involved in metabolism and warrant investigation of the possibility of clinical drug interactions mediated by inhibition of this enzyme. | Anwar A, McTernan PG, Anderson LA, Askaa J, Moody CG, Barnett AH, Eggo MC, Kumar S (2001)
Site-specific regulation of oestrogen receptor-alpha and -beta by oestradiol in human adipose tissue.
Diabetes, obesity & metabolism 3, 338-349 [PubMed:11703424]
[show Abstract]
AimTo examine the expression of oestrogen receptors alpha and beta (ERalpha and ERbeta) and their regulation by 17beta-oestradiol (E2) in stromal cells and adipocytes from human subcutaneous (s.c.) and omental (o.m.) adipose tissue.MethodsSubcutaneous and o.m. abdominal adipose tissues were obtained from 10 women (mean age 63.5 +/- 4.8 years; mean weight 75.6 +/- 6.7 kg) undergoing elective or cosmetic surgery. Immunohistochemistry and RT-PCR analysis were used to detect the presence of ERalpha and ERbeta. The regulation of ERalpha and ERbeta by E(2) (10(-7) M to 10(-9) M) was examined using Western immunoblotting analysis in both s.c. and o.m. stromal cells and mature adipocytes cultured in serum-free, phenol red-free medium.ResultsImmunostaining of s.c. and o.m. adipose tissue showed that the ER subtypes were localized predominantly within the nucleus. Western analysis demonstrated that E2 treatments differentially altered ERalpha and ERbeta expression in s.c. and o.m. adipocytes. In s.c. and o.m. stromal cells, E(2) (10(-8) M) produced a significant up regulation relative to control of 66 kDa ERalpha (s.c.:1.87 +/- 0.22; o.m.:1.97 +/- 0.17; p < 0.05) and 60 kDa ERbeta (s.c.:1.66 +/- 0.3; o.m.: 1.68 +/- 0.16; p < 0.05). In s.c. adipocytes, however, ERalpha expression significantly decreased with E(2) 10(-8) M relative to control while ERbeta expression increased (ERalpha 0.58 +/- 0.06, ERbeta: 1.47 +/- 0.11; p < 0.05). In o.m. adipocytes, the inhibition of ERalpha with E(2) was not observed (ERalpha 1.86 +/- 0.36, ERbeta:1.03 +/- 0.15, p < 0.05)ConclusionsERalpha and ERbeta are expressed but differentially regulated by E(2) in s.c. and o.m. adipocytes and stromal cells. The upregulation of ERbeta by E(2) suggests that E(2) maintains the expression of these receptors. The feed-back inhibition of ERalpha expression by E(2) in s.c. but not o.m. adipocytes observed in vitro is consistent with the data from ERalpha knock out mice where s.c. fat is increased. Selective ER modulators may have different effects in different adipose sites. | Pentikäinen V, Erkkilä K, Suomalainen L, Parvinen M, Dunkel L (2000)
Estradiol acts as a germ cell survival factor in the human testis in vitro.
The Journal of clinical endocrinology and metabolism 85, 2057-2067 [PubMed:10843196]
[show Abstract]
The necessity of estrogens for male fertility was recently discovered in studies on both estrogen receptor alpha knockout and aromatase (cyp 19 gene) knockout mice. However, direct testicular effects of estrogens in male reproduction have remained unclear. Here we studied the protein expression of ERalpha and the recently described estrogen receptor beta in the human seminiferous epithelium and evaluated the role of 17beta-estradiol, the main physiological estrogen, in male germ cell survival. Interestingly, both estrogen receptors alpha and beta were found in early meiotic spermatocytes and elongating spermatids of the human testis. Furthermore, low concentrations of 17beta-estradiol (10(-9) and 10(-10) mol/L) effectively inhibited male germ cell apoptosis, which was induced in vitro by incubating segments of human seminiferous tubules without survival factors (i.e. serum and hormones). Dihydrotestosterone, which, in addition to estradiol, is an end metabolite of testosterone, was also capable of inhibiting testicular apoptosis, but at a far higher concentration (10(-7) mol/L) than estradiol. Thus, estradiol appears to be a potent germ cell survival factor in the human testis. The novel findings of the present study together with the previously reported indirect effects of estrogens on male germ cells indicate the importance of estrogens for the normal function of the testis. | Ball WJ, Kasturi R, Dey P, Tabet M, O'Donnell S, Hudson D, Fishwild D (1999)
Isolation and characterization of human monoclonal antibodies to digoxin.
Journal of immunology (Baltimore, Md. : 1950) 163, 2291-2298 [PubMed:10438974]
[show Abstract]
Fab preparations of sheep polyclonal anti-digoxin Abs have proven useful for reversal of the toxic effects of digoxin overdoses in patients. Unfortunately, the use of foreign species proteins in humans is limited because of the potential for immunological responses that include hypersensitivity reactions and acute anaphylaxis. Immunization of recently developed transgenic mice, whose endogenous micro heavy and kappa light chain Ig genes are inactivated and which carry human Ig gene segments, with a digoxin-protein conjugate has enabled us to generate and isolate eight hybridoma cell lines secreting human sequence anti-digoxin mAbs. Six of the mAbs have been partially characterized and shown to have high specificity and low nanomolar affinities for digoxin. In addition, detailed competition binding studies performed with three of these mAbs have shown them to have distinct differences in their digoxin binding, and that all three structural moieties of the drug, the primary digitoxose sugar, steroid, and five-member unsaturated lactone ring, contribute to Ab recognition. | Murakami K, Nakagawa T, Shozu M, Uchide K, Koike K, Inoue M (1999)
Changes with aging of steroidal levels in the cerebrospinal fluid of women.
Maturitas 33, 71-80 [PubMed:10585175]
[show Abstract]
ObjectiveAge-related changes of steroid levels in the central nervous system (CNS) are not well understood. To investigate whether steroidal conditions in the CNS of women change with aging and menopause, steroid levels have been measured in serum and cerebrospinal fluid (CSF), and examined correlations with aging.MethodsSerum and CSF concentrations of estradiol (E2), cortisol, dehydroepiandrosterone (DHEA), DHEA sulfate (DHEAS) and albumin were measured in 80 female patients who underwent operations for benign gynecological diseases. They had no endocrinological or neurological disorders and were aged 17-71 years; 62 patients were in premenopause and 18 were in postmenopause.ResultsSerum levels of E2 decreased markedly after menopause, while levels of DHEA and DHEAS decreased gradually with age. There was no significant change with age of serum cortisol levels. The CSF concentrations of E2 (0.2-3 pg/ml) decreased with age [correlation coefficient (r)= 0.31, P < 0.01]. The CSF DHEA levels (0.1-0.8 ng/ml) did not change with age although not significantly, but CSF cortisol levels (0.1-0.6 microg/dl) increased with age (r = 0.35, P < 0.01). The CSF DHEAS concentrations were below the sensitivity of the radioimmunoassay (RIA) (1 ng/ml). The CSF/serum ratios of cortisol increased with age (r = 0.30, P < 0.01), as did those of DHEA (r = 0.55, P < 0.01). Although serum albumin levels did not change throughout life, CSF albumin levels and CSF/serum albumin ratios increased gradually with age (r = 0.28, P = 0.052; r = 0.23, P = 0.114, respectively), but there was no significance. There were marked decreases of serum E2 and DHEA levels and CSF E2 levels in postmenopausal women (P < 0.05), but CSF cortisol levels increased (P < 0.05) and DHEA levels in CSF were maintained after menopause.ConclusionThese results indicate that steroids in CSF become cortisol dominated and deficient in estrogens with aging, especially after menopause. | Blomquist CH, D'Ascoli PT (1995)
Gestational development of human placental 17 beta-hydroxysteroid oxidoreductase types 1 and 2.
Human reproduction (Oxford, England) 10, 2685-2689 [PubMed:8567793]
[show Abstract]
Human placenta is a rich source of 17 beta-hydroxysteroid oxidoreductase (17-HOR) type 1, a cytosolic enzyme highly specific for 17 beta-oestradiol, and type 2, a microsomal form reactive with both oestradiol and testosterone. Although a number of studies have established that 17-HOR activity is present in placenta as early as weeks 4-5 of gestation, more specific data on the pattern of development of these two enzyme forms are lacking. In this study, samples of villous tissue from weeks 7-20 of gestation were fractionated into cytosol and microsomes and 17-HOR activity assayed under conditions which differentiate between the two enzyme types. Type 1 activity with oestradiol of cytosol and microsomal type 2 activity with oestradiol and testosterone increased from week 7 to week 20. Activities at 17-20 weeks approximated those at 38-40 weeks. The high, cytosolic oestradiol/T activity ratio (160 +/- 20), characteristic of 17-HOR type 1, was constant between weeks 7 and 20, as was the low microsomal ratio (3.4 +/- 0.4) characteristic of the type 2 activity. There was a relationship between cytosolic type 1 activity and microsomal type 2 activity between weeks 7 and 20 (r = 0.59, P = 0.0055). These results indicate both activities increase coincident with the luteal-placental shift and that their temporal patterns of development are related between weeks 7 and 20 of gestation. | Sharpe RM, Skakkebaek NE (1993)
Are oestrogens involved in falling sperm counts and disorders of the male reproductive tract?
Lancet (London, England) 341, 1392-1395 [PubMed:8098802]
[show Abstract]
The incidence of disorders of development of the male reproductive tract has more than doubled in the past 30-50 years while sperm counts have declined by about half. Similar abnormalities occur in the sons of women exposed to diethylstilbestrol (DES) during pregnancy and can be induced in animals by brief exposure to exogenous oestrogen/DES during pregnancy. We argue that the increasing incidence of reproductive abnormalities in the human male may be related to increased oestrogen exposure in utero, and identify mechanisms by which this exposure could occur. | Fraser D, Padwick ML, Whitehead M, Coffer A, King RJ (1991)
Presence of an oestradiol receptor-related protein in the skin: changes during the normal menstrual cycle.
British journal of obstetrics and gynaecology 98, 1277-1282 [PubMed:1777462]
[show Abstract]
ObjectiveTo investigate the presence of an oestradiol receptor-related protein (P29) in skin and skin organelles, and to assess changes in its content during the normal menstrual cycle.DesignAn observational study.SettingKing's College School of Medicine and Dentistry, London.SubjectsTwenty-one premenopausal women with regular menstrual cycles undergoing gynaecological surgery. They were allocated to proliferative or secretory phases of the menstrual cycle on the basis of menstrual dating and histological examination of an endometrial sample.InterventionsSmall full thickness sections of skin (about 5 mm in depth) taken from the anterior abdominal wall at hysterectomy or laparoscopic sterilization.Main outcome measuresThe concentration of the oestradiol receptor-related protein in skin and its organelles was assessed semi-quantitatively, using a monoclonal antibody technique. The intensity of staining was compared between the proliferative and secretory phases of the cycle.ResultsThe receptor-related protein was consistently observed in epidermis, sebaceous glands, hair follicles and sweat ducts; there was no significant difference in its concentration between the proliferative and secretory phases of the menstrual cycle. The protein was not present in dermis and sweat ducts.ConclusionsEpidermis and some skin organelles contain an oestradiol receptor-related protein and must be considered as oestrogen target tissues. However, the content of this protein does not appear to change significantly during the normal menstrual cycle. | Bucala R, Lahita RG, Fishman J, Cerami A (1987)
Anti-oestrogen antibodies in users of oral contraceptives and in patients with systemic lupus erythematosus.
Clinical and experimental immunology 67, 167-175 [PubMed:3621671]
[show Abstract]
Recent studies have demonstrated that many patients with SLE have elevated plasma levels of the minor oestrogen metabolite 16 alpha-hydroxyestrone (16 alpha OHE). This oestrogen is unique in its ability to react with lysine residues and form stable, covalent Heyns products with proteins. Increased levels of 16 alpha OHE-modified proteins have been found to occur on the membranes of red cells and lymphocytes in patients with SLE. In the present study, patient and control sera were analysed for the presence of circulating immunoglobulins which react with an oestrogen hapten. Anti-oestrogen antibodies were detected in 26% (9/34) of male and female SLE patients, and were found to correlate both with levels of plasma 16 alpha OHE (P less than 0.001) and with the presence of active disease (P less than 0.005). Surprisingly, this antibody activity was also observed in 25% (13/52) of normal, disease-free women who had a history of oral contraceptive use. No detectable activity was observed in normal men, women who had not taken oral contraceptives, or patients with a variety of other immunological diseases. The possible role of anti-oestrogen antibodies in both the hormonal exacerbation of SLE and in the long-term sequelae of oral contraceptive usage is discussed. |
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