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PubMedDate not supplied

Systemic lupus erythematosus associated with klinefelter's syndrome.

Studies in estrogen metabolism were carried out in 2 males with systemic lupus erythematosus (SLE) who also had Klinefelter's syndrome. Although these studies revealed elevated levels of urinary estrogens in 1 patient, abnormalities of estradiol metabolism suggesting persistent estrogen stimulation were detected in both. This report notes an association between SLE and Klinefelter's syndrome and suggests that chronic estrogenic stimulation may be significant in the development of SLE in these 2 patients.

Adult↗
PubMed1995

Regulation of sex-hormone-binding globulin production by endogenous estrogens in vitro.

The effect of endogenous estrogens on sex-hormone-binding globulin (SHBG) production was studied in HepG2 cells. 17 beta-estradiol, estrone, and estrogens from both 2- and 16 alpha-hydroxylative pathways stimulated SHBG production, but not in parallel with their binding affinities for the estrogen receptor. Thus, the underlying mechanism may be other than a pure interaction with the estrogen receptor.

2-Methoxyestradiol↗
PubMed1998

Glucuronidation of catechol estrogens by expressed human UDP-glucuronosyltransferases (UGTs) 1A1, 1A3, and 2B7.

Catechol estrogens are major estrogen metabolites in mammals and are the most potent naturally occurring inhibitors of catecholamine metabolism. These estrogen compounds have been implicated in carcinogenic activity and the 4/2-hydroxyestradiol concentration has been shown to be elevated in neoplastic human mammary tissue compared to normal human breast tissue. Three human liver UDP-glucuronosyltransferases, UGT2B7, UGT1A1, and UGT1A3, have been shown to catalyze the glucuronidation of catechol estrogens and lead to their enhanced elimination via urine or bile. The present study was designed to study the kinetic interaction of expressed human UGT2B7(Y) or (H), UGT1A1, and UGT1A3 toward 2- and 4-hydroxycatechol estrogens. cDNAs encoding UGT2B7(Y) or (H), UGT1A1, and UGT1A3 were expressed in HK293 cells, and cell homogenates or membrane preparations were used to determine their glucuronidation ability. UGT2B7(Y) reacted with higher efficiency toward 4-hydroxyestrogenic catechols, whereas UGT1A1 and UGT1A3 showed higher activities toward 2-hydroxyestrogens. UGT2B7(H) catalyzed estrogen catechol glucuronidation with efficiencies similar to UGT2B7(Y). Flunitrazepam (FNZ), a competitive inhibitor of morphine glucuronidation in hepatic microsomes, competitively inhibited catechol estrogen glucuronidation catalyzed by UGT2B7(Y), UGT1A1, and UGT1A3. Buprenorphine, an opioid substrate that reacts at high efficiency with each of these UGTs, was also studied. FNZ competitively inhibited buprenorphine glucuronidation with UGT1A1 and UGT2B7 but had no inhibitory activity toward UGT1A3. This suggests that buprenorphine and 2-hydroxycatechol estrogens react with separate active sites of UGT1A3. A catecholamine, norepinephrine, did not inhibit UGT2B7(Y)-, UGT1A1-, and UGT1A3-catalyzed glucuronidation of catechol estrogens. These results also suggest that drug-endobiotic interactions are possible in humans and may have implication in carcinogenesis.

Estradiol↗
PubMed1991

Effect of catechol oestrogens on extraneuronal metabolism of noradrenaline by rabbit uterine endometrium and myometrium.

The effects of 2-hydroxy and 2-methoxy oestrogens on the extraneuronal O-methylation of 3H-(-)-noradrenaline were examined in progesterone-dominated, monoamine oxidase (MAO)-inhibited, rabbit uterine tissues in vitro. Both the corticosteroid-sensitive system in myometrium and the cocaine-sensitive system in endometrium were examined. In myometrial slices preincubated with nialamide to inhibit MAO and incubated with cocaine to inhibit neuronal uptake, 3H-normetanephrine (3H-NMN) formation was inhibited in the order of potency 2-hydroxy oestrone greater than or equal to 2-hydroxy oestradiol = 2-methoxy oestradiol greater than or equal to 2-methoxy oestrone. In myometrial slices not exposed to cocaine and nialamide, inhibition of 3H-NMN formation by both 2-hydroxy and 2-methoxy oestradiol did not affect the formation of deaminated metabolites of 3H-(-)-noradrenaline by the alternative metabolising pathway. In endometrial slices preincubated with nialamide to inhibit MAO, only 2-hydroxy oestrogens inhibited 3H-NMN formation, but they were one to two orders of magnitude less potent in this regard than in the myometrium. The uptake of 3H-(-)-noradrenaline by MAO- and COMT-inhibited myometrial slices was inhibited by 2-hydroxy and 2-methoxy oestrogens in the order of potency 2-methoxy oestradiol greater than or equal to 2-methoxy oestrone greater than or equal to 2-hydroxy oestrone greater than 2-hydroxy oestradiol. Uptake of 3H-(-)-noradrenaline by endometrial slices was not affected by either 2-hydroxy or 2-methoxy oestrogens.(ABSTRACT TRUNCATED AT 250 WORDS)

2-Methoxyestradiol↗
PubMed1986

Modulation of lectin-stimulated lymphocyte agglutination and mitogenesis by estrogen metabolites: effects on early events of lymphocyte activation.

Pharmacological doses of estrogens such as 17-beta estradiol (17-beta E) and diethylstilbestrol (DES) suppress cell-mediated immunity in vivo. In this report, we investigated the direct in vitro effects of 17-beta E and its major metabolites on lymphocyte proliferation in response to the T cell lectin phytohemagglutinin (PHA). PHA-induced lymphocyte agglutination, an early event indicative of active, cytoskeletal-dependent membrane alterations, was monitored in conjunction with blastogenesis. Without exception, the effects of individual estrogen metabolites on the PHA-induced agglutination occurring within minutes were accompanied, at every concentration of compound, by equivalent effects on the blastogenic response of activated cells measured after several days. This observation suggested a role for estrogens in modulating lymphocyte activation at the cell surface rather than through cytosolic receptor-mediated events. As suggested by previous studies with quinone metabolites of benzene, the catechol estrogen metabolite 2-OH estrone (2-OH E) was significantly more potent than the parent compound at suppressing lymphocyte proliferation in vitro and in vivo.

Agglutination↗
PubMed1991

Urinary excretion of catecholestrogens, 2-methoxy-estrogens and "classical estrogens" throughout the normal menstrual cycle.

Catecholestrogens, 2-methoxyestrogens and "classical" estrogens (estrone, estradiol, estriol) were measured simultaneously in urine samples of healthy women during the menstrual cycle. All estrogen values reach a preovulatory maximum at the time of the LH peak and show a marked increase during the luteal phase as compared to the follicular phase. Catecholestrogens and estrone seem to behave similarly supporting the assumption that catecholestrogens are predominantly metabolites of estrone. Daily measurements of urinary estrogens show large interindividual variations of 2- and 4-hydroxyestrogens as well as very differing 2-hydroxy-/2-methoxyestrogen ratios. The results obtained support the assumption, that catecholestrogens and their methylethers are excretory products with no additional regulatory functions.

2-Methoxyestradiol↗
PubMed2005

Hormone dependency of breast tumours developing in the Guernsey Cohort study.

The aim of this study was to determine whether endogenous estradiol levels in postmenopausal women helped determine the estrogen receptor status of subsequent breast cancers. Within the Guernsey Cohort study of 6127 women, 140 have been diagnosed with breast cancer of whom 59 had estradiol assays performed and ER status available. Estradiol levels in serum and urine were measured by radioimmunoassay and ER status of tumours by immunohistochemistry. Of the individuals in the highest tertile of serum estradiol 35% had ER+ve tumours compared with 27% in the lowest tertile. In terms of 16hydroxyestrone excretion the proportions ER+ve tumours were 22% in the lowest tertile and 38% in the highest tertile. This suggests that endogenous estrogen levels do impact on the phenotype of subsequent breast cancer.

Breast Neoplasms↗
PubMed1987

Novel and potent biological antioxidants on membrane phospholipid peroxidation: 2-hydroxy estrone and 2-hydroxy estradiol.

Catechol estrogens, 2-hydroxy estrone, 2-hydroxy estradiol and 2-hydroxy estriol, were tested as possible antioxidants of phospholipid peroxidation induced by Fe3+-ADP-adriamycin, using phospholipid liposomes as lipid source and alpha-tocopherol or other steroids as reference compounds. The parameters of antioxidant activities were: elongation of induction period, inhibition of O2 consumption required for lipid peroxidation and inhibition of peroxidative cleavage of unsaturated phospholipid. Of the tested compounds, 2-hydroxy estradiol or 2-hydroxy estrone had more potent activity than that of tocopherol.

Adenosine Diphosphate↗
PubMed1980

Kober reaction kinetics and their influence on the design of assays for oestrogens in urine during pregnancy.

Rates of reaction of different oestrogens in Kober reagent vary greatly. Rate constants were measured between 100 degrees C and 150 degrees C. Oestradiol, oestrone, 16-oxo-oestradiol, 16 alpha hydroxyoestrone, 16-epioestriol and urine pool show two sequential first order reactions at 100 degrees C; oestriol and its conjugates give a single reaction (slower than the other oestrogens except for the very slow oestretrol). Above 120 degrees C differences decrease, all oestrogens having one rate for Kober product formation: the decay reaction, which is also first order, becomes significant. Oestriol and its conjugates have relatively high apparent activation energies in the Kober reaction (120-138 kJmol-1) compared to other oestrogens studied (105-124 kJmol-1). The apparent activation energy for the decay reaction is the same within experimental error (115 +/- 3 kJmol-1). This is consistent with a common product formed from oestrogen reacting with Kober reagent. Analytical methods must respond similarly to major urinary oestrogens. Appropriate conditions include 100 degrees C for at least 20 min or 135 degrees C for 3 to 4 minutes.

Autoanalysis↗