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  • COMT
  • 12 Hydroxylated primary estrogens, especially the catecholestrogens (hydroxylated estrogens at the carbon 2 and 4 positions), undergo enzymatic O -methylation by catechol- O -methyltransferase (COMT) to form methoxyestrogens, such as 2-methoxyestrone, 3-methoxyestrone, 4-methoxyestrone, 2-methoxyestradiol, and 4-methoxyestradiol ( Figure 1 ). (ahajournals.org)
  • primary estrogens
  • however, whether primary estrogens can be useful biomarkers for maternal and fetal well being in adverse pregnancies, including preeclampsia, has been a subject of controversy. (ahajournals.org)
  • Several studies support evidence that serum and urinary primary estrogens may be useful for screening for adverse pregnancy outcomes, 8 whereas others contend that measurement of these estrogens is of little value. (ahajournals.org)
  • 11 Nevertheless, the levels and plasma profile of circulating primary estrogens in preeclampsia are, at best, unclear, and this is further complicated by the lack of information on estrogen metabolites, thus hindering our comprehensive understanding of their role(s) in its pathophysiology. (ahajournals.org)
  • Primary estrogens are converted in the uteroplacental unit by cytochrome P450s (CYP450s) into multiple hydroxylated metabolites defined by the position of hydroxylation, such as 2-hydroxyestrone, 4-hydroxyestrone, 16-α-hydroxyestrone, 2-hydroxyestradiol, and 4-hydroxyestradiol ( Figure 1 ). (ahajournals.org)
  • enzymes
  • Polymorphisms in maternal or offspring genes encoding estrogen-metabolizing enzymes may influence prenatal catechol estrogen levels and could therefore be biomarkers of TGCC risk. (aacrjournals.org)
  • Variation in maternal or offspring genes encoding estrogen-metabolizing enzymes could influence the level of exposure to prenatal catechol estrogens and could therefore serve as biomarkers in a retrospective study of hormonal risk factors for TGCC. (aacrjournals.org)
  • The steroid is known to compete with catecholamines for binding to catechol O-methyltransferase and tyrosine hydroxylase and to directly and competitively inhibit these enzymes. (wikipedia.org)
  • reactive estrogen
  • 2-Hydroxyestradiol, as well as 2-hydroxyestrone and 4-hydroxyestradiol, can undergo metabolic redox cycling to generate free radicals like superoxide and reactive estrogen semiquinone/quinone intermediates. (wikipedia.org)
  • CYP1B1
  • We conducted a population-based, case-parent triad study ( 16 ) to test whether TGCC risk is related to maternal and/or offspring variation in genes involved in catechol estrogen formation ( CYP1A2, CYP1B1, CYP3A4 , and CYP3A5 ). (aacrjournals.org)
  • tissues
  • Mammalian adult male germ cells and supporting gonadal tissues are highly susceptible to the toxic effects of ROS ( 9 - 12 ), and catechol estrogens seem to be involved in some of these toxic effects ( 13 , 14 ). (aacrjournals.org)
  • LE2 are highly lipophilic and hydrophobic and are found in highest concentrations in adipose tissue and other estrogen-sensitive tissues and in low but detectable concentrations in circulation, with none excreted in urine. (wikipedia.org)
  • However, 2-hydroxyestradiol shows little or no tumorigenic activity in the male Syrian hamster kidney and there is evidence that 2-hydroxyestradiol may actually decrease tumorigenesis in estrogen-sensitive tissues. (wikipedia.org)
  • risk of endometrial cancer
  • Analysis of the joint effects of genotype and markers of estrogen exposure found the lowest risk of endometrial cancer among those with the homozygous variant genotype of the rs2070959 polymorphism and who were postmenopausal, had low body mass index, and had low soy food intake, although a test for multiplicative interaction was not significant. (aacrjournals.org)
  • Taken together, these data suggest that the G/G genotype ( rs2070959 ) in the UGT1A1 gene may decrease the risk of endometrial cancer and that this effect is most evident among women with low levels of endogenous estrogen exposure or with low soy food intake. (aacrjournals.org)
  • progestin
  • Hormone therapy, estrogen plus progestin (E+P) particularly, is associated with increased risk of breast cancer. (aacrjournals.org)
  • Epidemiologic studies have also provided strong evidence that postmenopausal hormone therapy use, particularly the use of estrogen plus progestin (E+P), is associated with increased breast cancer risk ( 3 - 6 ). (aacrjournals.org)
  • giving a progestin with an estrogen mitigates the risk. (wikipedia.org)
  • exposure
  • Exposure to relatively high circulating maternal estrogen levels during pregnancy has long been suspected as being a risk factor for TGCC. (aacrjournals.org)
  • Estrogen exposure-related factors evaluated include menstrual characteristics, oral contraceptive use, body mass index, waist-hip ratio, and soy food intake. (aacrjournals.org)
  • Specifically, endogenous estrogens, such as unopposed estrogen therapy, as well as markers of endogenous estrogen exposure, such as nulliparity, early menarche, late menopause, and obesity, have all been shown to increase endometrial cancer risk ( 1 - 9 ). (aacrjournals.org)
  • While some studies in the early 1990s claimed a connection between globally declining sperm counts and estrogen exposure in the environment, later studies found no such connection, nor evidence of a general decline in sperm counts. (wikipedia.org)
  • whereas
  • For instance, 2-hydroxyestrone reportedly shows negligible uterotrophic effect in animals, whereas 4-hydroxy catechol estrogens show moderate changes in stimulating uterine weight. (wikipedia.org)
  • reactive
  • Under poor conditions of inactivation by phase II enzymes, catechol estrogens can undergo oxidation to reactive quinones and semiquinones, and this has been hypothesized to contribute to estrogen-induced carcinogenesis. (wikipedia.org)
  • 2-Hydroxyestradiol, as well as 2-hydroxyestrone and 4-hydroxyestradiol, can undergo metabolic redox cycling to generate free radicals like superoxide and reactive estrogen semiquinone/quinone intermediates. (wikipedia.org)
  • hormonal
  • Senyawa estrogen-katekol bisa duwén sipat tumorigenik utawa anti-tumorigenik, upamané 4-hydroxyestradiol duwé sipat hormonal kanti ngaktivasi pencerap estrogen, lan nginduksi adenokarsinoma ing endometrium . (wikipedia.org)
  • liver
  • Raxworthy MJ, Gulliver PA, Hughes PJ (1982) The cellular location of catechol-O-methyltransferase in rat liver. (springer.com)
  • 2-Hydroxyestradiol has been identified as a prodrug of 2-methoxyestradiol, a transformation which is very efficiently catalyzed by catechol O-methyltransferase in the liver. (wikipedia.org)
  • hormone
  • 163, 1959, 47: 1-101) he was able to show that the production of estrogen in the ovaries is dependent on an interplay of two different hormone producing systems. (wikipedia.org)
  • In one, a precursor - a variant of the male sex hormone - is formed, that is then transformed to estrogen in the second system. (wikipedia.org)
  • breakdown
  • Another example of historical significance relating to transferase is the discovery of the mechanism of catecholamine breakdown by catechol-O-methyltransferase. (wikipedia.org)
  • Presence
  • Roth SA (1980) Presence of membrane-bound catechol-O-methyltransferase in human brain. (springer.com)
  • interestingly, in the presence of ascorbate to inhibit autoxidation, these catechols were formed quantitatively. (uic.edu)
  • formulations
  • Estrone was previously marketed in intramuscular and vaginal formulations and was used as an estrogen in the treatment of symptoms of hypoestrogenism such as hot flashes and atrophic vaginitis in menopausal or ovariectomized women. (wikipedia.org)
  • women
  • In the 1930s, estrone was given via intramuscular injection to ovariectomized women in order to study its effects and to elucidate the biological properties of estrogens in humans. (wikipedia.org)
  • response
  • implicated 4-OH-E2 in the induction of estrogen-responsive genes, a response that exhibited partial or no abrogation by coadministration with an antiestrogen, providing evidence for the ability of 4-OH-E2 to carry out genetic upregulation via a pathway independent of ER signalling. (wikipedia.org)