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PubMed1992

Induction by estrogen metabolite 16 alpha-hydroxyestrone of genotoxic damage and aberrant proliferation in mouse mammary epithelial cells.

BACKGROUND: Estrogens are potent mammary tumor promoters influencing post-initiation events via epigenetic mechanisms. The upregulation (i.e., induction) of the C16 alpha-hydroxylation pathway during 17 beta-estradiol (E2) biotransformation has been associated with mammary cell transformation. The action of E2 metabolites on tumorigenic transformation, however, is poorly understood. PURPOSE: The newly established mammary epithelial cell line C57/MG, derived from the C57BL mouse strain, was used to examine whether E2 or its metabolites, 16-hydroxyestrone (16 alpha-OHE1) and estriol (E3), function as initiators of mammary cell transformation. METHODS: DNA repair (hydroxyurea-insensitive thymidine uptake), estrogen metabolism (3H exchange to form 3H2O), hyperproliferation (increased cell number), and acquisition of anchorage-independent growth (soft-agar colonies) were used as quantitative end points to measure the relative extent of transformation. RESULTS: Treatment of cells with 200 ng/mL 16 alpha-OHE1 resulted in a 55.2% increase in DNA repair synthesis, a 23.09% increase in proliferative activity, and a 18-fold increase in the number of soft-agar colonies, relative to the solvent controls (P less than .0001). The extent of upregulation of the three end points was similar to that induced by the genotoxic mammary carcinogen 7, 12-dimethylbenz[a]anthracene (DMBA, positive control). DMBA treatment also upregulated the ratio of 16 alpha/C2 hydroxylation of E2 leading to increased formation of 16 alpha-OHE1. E2 and E3 were not effective in upregulating these markers for transformation. CONCLUSION: These results demonstrate that in nontransformed C57/MG cells, 16 alpha-OHE1 may function as an initiator, perturbing the intermediate biomarkers for preneoplastic transformation.

Animals↗
PubMed1984

The reaction of 16 alpha-hydroxyestrone with erythrocytes in vitro and in vivo.

16 alpha-Hydroxyestrone (16 alpha OHE ) has been shown previously to react with albumin, forming stable covalent adducts with lysine residues. The incubation of [3H]16 alpha OHE with whole blood also results in the incorporation of tritium into cells, with the rate of incorporation paralleling that of 16 alpha OHE -protein adduct formation. 32% of erythrocyte acid-precipitable radioactivity was found to be present within membrane proteins and electrophoresis demonstrated that several of these proteins are modified by [3H]16 alpha OHE . Membrane proteins from the red cells of ten individuals were reduced with sodium borohydride, acid hydrolyzed, and the 16 alpha OHE -lysine adducts purified by hydrophobic chromatography and reverse-phase high-pressure liquid chromatography. The amount of these adducts was quantitated by radioimmunoassay and found to be five times higher than the plasma levels of free 16 alpha OHE . This reflects most likely the accumulation of 16 alpha OHE -protein adducts during the course of the red cell life. Quantitation of 16 alpha OHE -protein adducts with other cellular proteins may contribute to our understanding of systemic lupus erythematosus, an autoimmune disease in which elevated levels of 16 alpha OHE occur.

Blood Proteins↗
PubMed1980

Suppression of prolactin secretion in normal young women by 2-hydroxyestrone.

The nonuterotropic natural estrogen 2-hydroxyestrone administered to normal young women results in a prompt and profound suppression of serum prolactin in most of the subjects. With the exception of dopamine, this is the only endogenous material known to strongly inhibit prolactin secretion, and its action suggests that the physiological regulation of prolactin by estrogens in the human is dual in nature, consisting of stimulation by estradiol and inhibition by its catechol estrogen metabolite.

Adult↗
PubMed1981

Metabolic clearance rate and uterotropic activity of 2-hydroxyestrone in rats.

2-Hydroxyestrone (2-OHE1) has much lower uterotropic potency than might be predicted from its uterine estrogen receptor affinity. 2-OHE1 displaces saturably bound [3H]estradiol from rat uterine cytosol with a competitive inhibition constant of 8.6 nM, while the dissociation constant for 17 beta-estradiol (E2) is 0.42 nM. From this ratio of binding affinities, one would expect some agonist or antagonist activity of 2-OHE1 to be apparent at doses roughly 20-50 times the minimum effective dose of E2. Instead, at doses of 2-OHE1 1000 times an effective dose of E2, no uterotropic effect was observed. When 2-OHE1 was injected together with E2 at dose ratios of 500:1, there was no antagonism of the effect of E2. To examine this discrepancy, the plasma MCRs (MCRpS) of E2 and 2-OHE1 were determined by continuous infusion techniques. Plasma concentrations of 2-OHE1 and E2 during control and infusion periods were measured by RIAs. The MCRp of 2-OHE1 averaged 50,000 ml/h, more than 100 times that of E2 (approximately 400 ml/h). The extraordinarily high MCRp of 2-OHE1 may explain the failure to observe any biological effects of this catechol estrogen, even at high doses. This rapid metabolism, presumably occurring in the blood compartment, should be considered in handling blood samples for RIA and in devising studies of the actions of catechol estrogens.

Animals↗
PubMed1983

Radioimmunoassay of 2-hydroxyestrone in plasma during the estrous cycle of the rat: interrelationships with estradiol, progesterone, and the gonadotropins.

A RIA for 2-hydroxyestrone (2-OHE1) in rat plasma has been developed. The assay employs an antiserum that is specific for catechol estrogens. Specificity is further ensured by purification of plasma extracts on Sephadex LH-20 columns before RIA. Blood was collected at 0 C in the presence of ascorbic acid to prevent oxidation. Under these conditions, the conversion of 2-OHE1 to methylated derivatives was found to be negligible. Plasma 2-OHE1, LH, FSH, PRL, estradiol, and progesterone were measured at 3-h intervals throughout the 4-day estrous cycle of the rat. The 2-OHE1 concentration varied from undetectable to 11 pg/ml plasma. No clearly defined relationship with the other hormones analyzed was observed. Thus, it is unlikely that changes in circulating 2-OHE1 levels are involved in the regulation of the gonadotropin surge and ovulation.

Animals↗
PubMed1984

Suppression of the preovulatory luteinizing hormone surge in the rat by 2-hydroxyestrone: relationship to endogenous estradiol levels.

Injection of 100 micrograms 2-hydroxyestrone (2OHE1) at various times on the morning of proestrus into normal 4-day-cycling rats results in abolition of the preovulatory LH surge in a number of animals tested. The greatest response was observed when the administration of 2OHE1 coincided with endogenous estradiol (E2) levels that were close to but not at their maximal proestrous levels. The catechol estrogen failed to abolish the LH surge if given much earlier or after the E2 maximum had already been reached. The effectiveness of 2OHE1 inhibition of the LH surge was greatly increased by the administration of 1 microgram E2 1 h before the catechol estrogen. 2OHE1 did not interfere with LH secretion in response to LHRH administration, indicating that the inhibitory action of the catechol estrogen is exercised at the hypothalamic level. In contrast to its inhibition of the positive feedback, 2OHE1 administered either before or after the injection of E2 to ovariectomized rats had no effect on the negative feedback of the hormone on pituitary LH secretion. The narrow and specific "time window" on proestrus when an injection of 2OHE1 results in the abolition of the preovulatory LH surge and its relation to the endogenous E2 preovulatory secretion suggest that the catechol estrogen interferes with a brief neuronal triggering event obligatory for LHRH release. The evidence also indicates that this action does not involve conventional competition for the E2 receptor.

Animals↗
PubMed1989

Differential effects of estradiol and 16 alpha-hydroxyestrone on pituitary and preoptic estrogen receptor regulation.

16 alpha-Hydroxyestrone (16OHE1), an endogenous metabolite of estradiol (E2), binds to the estrogen receptor (ER) with low affinity, but is estrogenic in various bioassay systems. 16OHE1 binds covalently to the ER in vitro, exhibits prolonged estrogenic bioactivity in vivo, and has been implicated in several estrogen-dependent diseases. This study examined the effects of 13 days of continuous infusion of E2 or 16OHE1 on lordotic behavior, pituitary growth, and ER regulation in the cytosolic and nuclear fractions of the pituitary and preoptic area of both sexes. Finally, simultaneous pituitary nuclear exchange assays and enzyme immunoassays were performed to search for covalent 16OHE1-ER complexes in vivo. E2 induced lordosis and pituitary growth in both sexes, while 16OHE1 was only slightly less effective. While E2 treatment increased nuclear ER concentrations 2-fold vs. control values, it decreased both cytosolic and total (cytosolic plus nuclear) ER concentrations in pituitary and preoptic area by approximately 3-fold vs. control values in both sexes by exchange assay. In contrast, 16OHE1 did not decrease total pituitary ER concentrations and only minimally decreased total preoptic ER concentrations. Simultaneous exchange assay and immunoassay of pituitary nuclear extracts demonstrated proportionate increases in ER levels in female vs. male and in E2-treated vs. 16OHE1-treated rats. The ratios of (ER enzyme immunoassay divided by ER-exchange) for each rat were similar regardless of metabolite administration. The correlation of individual measurements implied that ER localized to the nuclear fraction by either E2 or 16OHE1 retained both exchangeability and immunoassayability to similar extents, but did not support the presence of 16OHE1-ER covalent complexes. The results of this study suggest that 16OHE1 has significant estrogenic bioactivity, as manifest by its effects on lordosis and pituitary growth, but, in contrast to E2, does not decrease pituitary ER concentrations and only minimally decreases preoptic ER concentrations. This property may be important in the proposed pathogenetic action of 16OHE1 in estrogen-dependent disease.

Aging↗
PubMed1980

Biological properties of 16 alpha-hydroxyestrone: implications in estrogen physiology and pathophysiology.

Metabolism of estradiol in men with cirrhosis and subjects with systemic lupus erythematosus results in an excessive formation of 16 alpha-hydroxyestrone. Examination of the biological activity of this metabolite showed that it is a potent uterotropic agent and that it exhibits minimal affinity for the human sex hormone-binding globulin. These biological characteristics are consistent with a hyperestrongenic response to the substance, which may be reflected in the pathology and etiology of these diseases.

Animals↗
PubMed1980

Rapid metabolic clearance of the catechol estrogen 2-hydroxyestrone.

The plasma metabolic clearance rate (MCRp) of 2-hydroxyestrone was measured in normal young adults by two methods: infusion of unlabeled 2-OHE1 to equilibrium with radioimmunoassay of plasma 2-OHE1 levels, and infusion of [3H]2-OHE1 to equilibrium with measurement of chromatographically purified plasma [3H]2-OHE1. MCR's were 40--70,000 L/day and 15--50,000 L/day, respectively. This is the highest known MCR for a naturally occurring steroid. The only measurable plasma metabolite of [3H]2-OHE1 co-migrated with 2-methoxyestrone. When [3H]2-OHE1 was incubated with blood samples in vitro, [3H] xi-methoxyestrone was rapidly formed. Since this MCR is higher than cardiac output, clearance must occur primarily in the blood compartment, probably largely by the action of erythrocyte catechol-0-methyltransferase.

Adult↗
PubMed1985

Increased levels of 16 alpha-hydroxyestrone-modified proteins in pregnancy and in systemic lupus erythematosus.

The ketolic estrogen 16 alpha-hydroxyestrone (16 alpha OHE) reacts with lysine residues, forming stable covalent adducts with proteins. To determine the extent of protein modification by 16 alpha OHE in vivo, we measured the level of 16 alpha OHE-lysine present within proteins of varying half-lives obtained from normal subjects, patients with systemic lupus erythematosus (SLE), and pregnant women. The latter groups have higher than normal levels of plasma 16 alpha OHE. The proteins analyzed were membrane proteins of the red cell and the lymphocyte and basement membrane proteins of the glomerulus. We report that elevated levels of plasma 16 alpha OHE led to increased formation of 16 alpha OHE-protein adducts and that the level of these adducts increases with the half-life of the protein. In the case of erythrocyte membrane proteins, pregnant women and women with SLE had significantly higher mean levels of 16 alpha OHE-lysine than normal women (normal, 5.2 pmol 16 alpha OHE-lysine/mmol leucine; SLE, 15.7; pregnant, 24.9). A similar elevation in the modification of lymphocyte proteins in women was found (normal, 15.6; SLE, 40.5). Since the degree of protein modification also was dependent on the ambient level of free 16 alpha OHE, these measurements provide a useful indicator of the long term 16 alpha OHE status of an individual. The modification of proteins by 16 alpha OHE may be a link in the relationship between female hormones, pregnancy, and systemic lupus erythematosus.

Adolescent↗
PubMed1984

[Determination of free and conjugated 16 alpha-hydroxyestrone (16 alpha-OH E1) in serum by mass fragmentography using gas chromatography mass spectrometry].

A simple, rapid and highly specific method for the determination of maternal and cord serum 16 alpha-hydroxyestrone (16 alpha-OH E1) during pregnancy and at delivery was developed by mass fragmentographic technique using a Gas chromatography--Mass spectrometry (GC-MS) with application of deuterated estradiol as an internal standard. The equipment used was Shimadzu LKB9000 GC-MS (MID-PM). The T.F.A. derivative of the compounds was analyzed using the GC-MS system equipped with a 1 m glass coil, 1% OV-1 on chromosorb w 60 approximately 80 mesh. The flow rate of carrier gas (helium) was 25 ml/min. The temperatures of column oven, separator and ionization source were kept at 190 degrees C, 270 degrees C and 290 degrees C, respectively. The ionization energy and trap current were 70 eV and 60 microA, respectively. The mass spectrum showed molecular ions at m/ e467 and m/ e478 corresponding to the T.F.A. derivatives of d3-E2 and 16 alpha-OH E1 respectively. Evaluation of the method assessed by recovery experiments was 99.2 percent when 10 ng of 16 alpha-OH E1 was added to 1.0 ml of male serum treated with charcoal. The coefficient of variation was 4.2 percent. Serum conjugated 16 alpha-OH E1 levels during pregnancy increased with progressing gestation. The levels in early pregnancy (5th approximately 15th week), middle pregnancy (16th approximately 27th week) and late pregnancy (28th approximately 42th week) were 1.72 +/- 0.43 ng/ml, 5.35 +/- 2.60 ng/ml, 11.92 +/- 3.93 ng/ml (mean +/- S.D.), respectively. Mean levels of 16 alpha-OH E1 in the umbilical artery were 11.61 +/- 5.17 ng/ml which were statistically higher than these in the maternal peripheral vein (6.06 +/- 4.72 ng/ml) and umbilical vein (9.16 +/- 3.77 ng/ml). Serum 16 alpha-OH E1 levels in the samples obtained from anencephalic pregnancy were significantly lower than those in normal pregnancy, suggesting that fetal adrenal function may be involved in the formation of this steroid during pregnancy.

Chromatography, Gas↗
PubMed2001

Regulation of cell cycle and cyclins by 16alpha-hydroxyestrone in MCF-7 breast cancer cells.

It has been suggested that alterations in estradiol (E(2)) metabolism, resulting in increased production of 16alpha-hydroxyestrone (16alpha-OHE(1)), is associated with an increased risk of breast cancer. In the present study, we examined the effects of 16alpha-OHE(1)on DNA synthesis, cell cycle progression, and the expression of cell cycle regulatory genes in MCF-7 breast cancer cells. G(1) synchronized cells were treated with 1 to 25 nM 16alpha-OHE(1) for 24 and 48 h. [(3)H]Thymidine incorporation assay showed that 16alpha-OHE(1) caused an 8-fold increase in DNA synthesis compared with that of control cells, whereas E(2) caused a 4-fold increase. Flow cytometric analysis of cell cycle progression also demonstrated the potency of 16alpha-OHE(1) in stimulating cell growth. When G(1) synchronized cells were treated with 10 nM 16alpha-OHE(1) for 24 h, 62+/-3% of cells were in S phase compared with 14+/-3% and 52+/-2% of cells in the control and E(2)-treated groups respectively. In order to explore the role of 16alpha-OHE(1) in cell cycle regulation, we examined its effects on cyclins (D1, E, A, B1), cyclin dependent kinases (Cdk4, Cdk2), and retinoblastoma protein (pRB) using Western and Northern blot analysis. Treatment of cells with 10 nM 16alpha-OHE(1) resulted in 4- and 3-fold increases in cyclin D1 and cyclin A, respectively, at the protein level. There was also a significant increase in pRB phosphorylation and Cdk2 activation. In addition, transient transfection assay using an estrogen response element-driven luciferase reporter vector showed a 15-fold increase in estrogen receptor-mediated transactivation compared with control. These results show that 16alpha-OHE(1) is a potent estrogen capable of accelerating cell cycle kinetics and stimulating the expression of cell cycle regulatory proteins.

Breast Neoplasms↗
PubMed2005

Differential effects of 16alpha-hydroxyestrone and 2-methoxyestradiol on cyclin D1 involving the transcription factor ATF-2 in MCF-7 breast cancer cells.

We studied the effects of 2-methoxyestradiol (2-ME2) and 16alpha-hydroxyestrone (16alpha-OHE1), two metabolites of estradiol (E2), on DNA synthesis, cell cycle progression and cyclin D1 protein levels in estrogen receptor-positive MCF-7 cells. E2 and 16alpha-OHE1 stimulated DNA synthesis, and 2-ME2 inhibited the stimulatory effects of these agents. E2 and 16alpha-OHE1 stimulated the progression of cells from G1 to S phase and this effect was attenuated by 2-ME2. Western blot analysis showed that E2 and 16alpha-OHE1 increased cyclin D1 protein level by about fourfold compared with control. 2-ME2 had no significant effect on cyclin D1; however, it prevented the accumulation of cyclin D1 in the presence of E2 and 16alpha-OHE1. Cells transfected with a cyclin D1 reporter gene and treated with E2 or 16alpha-OHE1 showed 7- and 9.5-fold increase respectively in promoter activity compared with control. This activity was significantly inhibited by 2-ME2. Cyclin D1 transactivation was mediated by the cAMP response element (CRE) region, which binds activating transcription factor 2 (ATF-2). DNA affinity assay showed 2.5- and 3.5-fold increases in ATF-2 binding to CRE in the presence of E2 and 16alpha-OHE1 respectively. The binding of ATF-2 was inhibited by the presence of 2-ME2. These results show that 2-ME2 can downregulate cyclin D1 and thereby cell cycle progression by a mechanism involving the disruption of ATF-2 binding to cyclin D1 promoter.

2-Methoxyestradiol↗
PubMed1986

[Determination of serum 16 alpha-hydroxydehydroepiandrosterone, 16 alpha-hydroxyestrone and estriol by gas chromatography-mass spectrometry and their perinatal movement].

In order to study the mechanism of estriol (E3) formation in the fetoplacental unit, a method for determining E3 and its precursors, 16 alpha-hydroxydehydroepiandrosterone (16 alpha-OH DHA) and 16 alpha-hydroxyestrone (16 alpha-OH E1) in blood using Gas Chromatography-Mass Spectrometry (GC-MS) was newly developed. Deuterium labelled steroids, 3.4.4.-d3-16 alpha-OH DHA 2.4.17.-d3-E2 and 2.4.-d2-E3 were synthesized and used as the internal standards. After removal of free steroids with ether, the residue was solvolyzed and extracted with ethyl acetate as free form. Steroids were analysed after the formation of T.M.S. and T.F.A. derivative. The values for each steroid in maternal peripheral vein blood (M.V.), umbilical artery blood (U.A.) and vein blood (U.V.) were studied. Conjugated steroid values in M.V. obtained at normal vaginal delivery (13 cases) were as follows: 16 alpha-OH DHA 230.3 +/- 76.3 ng/ml, 16 alpha-OH E1 19.34 +/- 7.00 ng/ml and E3 158.8 +/- 50.2 ng/ml (mean +/- S.D.), respectively. The levels of these three steroids in cord blood were significantly higher than those in maternal blood. These results show that the steroids are actively produced in the fetoplacental unit. A significant increase in all the steroids was associated with labor. None of the values for E3 precursors in umbilical blood correlated with that of conjugated E3 in maternal blood. The significance of 16 alpha-OH DHA and 16 alpha-OH E1 as intermediates of E3 formation in the fetoplacental unit is discussed.

Dehydroepiandrosterone↗
PubMed1985

[Studies on RIA of 16 alpha-hydroxyestrone and its clinical application].

UNLABELLED: 16 alpha-hydroxyestrone (16 alpha-OH-E1) is an important intermediary metabolite in the biosynthetic pathway leading to estriol. No established routine method has been published to measure this steroid in the organism. A new RIA 16 alpha-OH-E1 method was developed and by using this method some interesting clinical data were obtained. METHOD: Rabbits were immunized with 16 alpha-OH-E1-3-CME-BSA to produce its antiserum. 16 alpha-OH-E1-3H was synthesized by incubating estrone-3H with the human fetal liver preparation and NADPH. As samples, peripheral blood of pregnant women, umbilical artery blood (UA), umbilical vein blood (UV) and amniotic fluid were collected. To each sample, 1000 dpm of 16 alpha-OH-E1-3H was added as a tracer, extracted with ether, and the extract was separated on TLC and LH-20. The 16 alpha-OH-E1 fraction was collected and used for RIA. RESULTS: The 16 alpha-OH-E1 levels (ng/ml) in peripheral maternal blood of normal gestation before 11 weeks, 12-23 weeks, 24-36 weeks and after 37 weeks were 0.98 +/- 0.07 (mean +/- S.E.), 2.42 +/- 0.30, 4.76 +/- 0.42 and 5.49 +/- 0.98, respectively. A significant increase in the steroid titer was observed as gestational weeks advanced.(ABSTRACT TRUNCATED AT 250 WORDS)

Amniotic Fluid↗
PubMed1982

[Specific radioimmunoassay and physiological significance of unconjugated 2-hydroxyestrone and 2-hydroxyestradiol-17 beta in human blood (author's transl)].

Recently it has been attached importance to the physiological function of catecholestrogens. To elucidate it a specific radioimmunoassay of conjugated 2-hydroxyestrone (2-OHE1) and 2-hydroxyestradiol-17 beta (2-OHE2) in human plasma was attempted. After extracting with ethyl acetate, samples were purified by a short Sephadex LH-20 columnchromatography and determined using the antiserum to 2-OHE1-17(O-carboxymethyl) oxime-bovine serum albumin conjugate. The following results were obtained: 1) A long Sephadex LH-20 columnchromatography which was used for the purification of catecholestrogens produced chemically, had a superior faculty in separation and high capacity 2) The antiserum cross-reacted 26.4% with 1-OHE2, but less than 1% with other steroid hormones. 3) The sensitivity of the method was around 10pg in both 2-OHE1 and 2-OHE2 assays. The method blank determined using 2ml plasma of bilaterally adreno-oophrectomized women was below 15 pg/ml in both 2-OHE1 and 2-OHE2 assays (n = 24). 4) The coefficient of variation in both accuracy and between-assay precision of the method was less than 17%. 5) The plasma 2-OHE1 concentration was below 15 pg/ml in normal men (n = 8) and non-pregnant women (n = 13). The concentration in pregnant women was 20 +/- 8 pg/ml (SD, n = 7) in 1st trimester of pregnancy, 58 +/- 13 (n = 3) in 2nd trimester and 177 +/- 66 (n = 12) in 3rd trimester. The E1/2-OHE1 and E2/2-OHE1 ratios in 3rd trimester of 9 pregnant women were 19.7 +/- 11.9(SD) and 78.0 +/- 27.8, respectively. 6) The plasma 2-OHE2 concentration was below 15 pg/ml in normal men (n = 8), non-pregnant women (n = 8), and 1st to 2nd trimester (n = 10) and 15 +/- 9 pg/ml (SD, n = 13) in 3rd trimester of pregnant women.

Adult↗
PubMed1984

[Changes in plasma 2-hydroxyestrone levels in pubertal females and correlation with sex hormones].

Plasma levels of 2-hydroxyestrone (2-OHE1) were measured by specific radioimmunoassay during puberty to elucidate the physiological role of this hormone on female sexual development. Plasma levels of FSH, LH, PRL and estradiol (E2) were also measured with an RI-kit. 67 girls between aged 6 and 16 were selected for this study. Blood samples were collected into tubes containing 0.1W/V% EDTA and 0.1W/V% ascorbic acid and immediately centrifuged. 2-OHE1 in plasma was extracted and separated with a Sephadex LH-20 column. RIA was applied using anti 2-OHE1-17-CMO-BSA. Plasma 2-OHE1 levels before menarche were low (6-7 pg/ml) until 10 years of age. The levels started to increase from 11 and reached 11.2 +/- 5.8pg/ml at 16 years of age. The levels of 2-OHE1 in girls after menarche were significantly higher than that before menarche (p less than 0.01). There was a significant correlation between 2-OHE1 and E2 in girls before menarche (p less than 0.001, r = 0.5416). However, the 2-OHE1 to E2 ratio decreased significantly from 9 to 10 years of age. These results indicate that during this period, the E2 increase is more predominant than that of 2-OHE1. There was a significant negative correlation between 2-OHE1 and PRL after menarche while no correlation between 2-OHE1 and FSH, LH was noticed. These results suggested that 2-OHE1 may play a role in sexual development after menarche rather than in the initiation of menarche.

Adolescent↗
PubMed1983

[Serum unconjugated 2-hydroxyestrone and erythrocyte catechol-O-methyltransferase activity in pregnancy toxemia].

To clarify the significance of catecholestrogens in toxemia of pregnancy, plasma unconjugated 2-hydroxyestrone (2-OHE1) was measured by a specific radioimmunoassay. In addition, catechol-O-methyltransferase (COMT) activity in erythrocytes was compared between normal and toxemic pregnancies. The following results were obtained. There was no significant difference in the plasma 2-OHE1 level between normal and toxemic pregnancies in the 3rd trimester, these being 220 +/- 53(SD,n = 7), 162 +/- 138(n = 9) pg/ml, respectively. However, the plasma 2-OHE1, level was quite low in all three subjects in toxemic pregnancy with placental dysfunctions. Liver dysfunction was found in only one case of toxemic pregnancy, whose plasma 2-OHE1 was within the normal range. In two cases of mild toxemia and one case of severe toxemia with placental dysfunctions there was no significant difference in COMT activity as compared with normal pregnancy. The COMT activity of a diabetic woman with pregnancy toxemia without placental dysfunctions was slightly higher than that of a normal pregnant woman. From these results it is suggested that the lower plasma 2-OHE1 level in toxemic pregnancy may be caused by placental dysfunctions.

Catechol O-Methyltransferase↗