Disease relevance of estrone

• The concentrations of testosterone (T), androstenedione (A), estradiol (E2), and estrone (E1) were measured in peripheral and ovarian venous serum obtained at the time of bilateral oophorectomy from 15 postmenopausal women with endometrial cancer and 9 without cancer [1].
• E1 was higher in the subjects with ESRD than in the control subjects at baseline (P < 0.05) [2].
• Thus, massive obesity is associated with abnormalities in hormonal balance in gynecologically symptomless women, there being an association between E1, E2, A, LH, cortisol, and relative weight and/or abdominal fat cell size [3].
• Subsequent to moderate weight reduction (13.2 kg), serum A and E1 levels (P less than 0.01) increased, and serum cortisol levels decreased (P less than 0.001) [3].
• These preliminary results do not support the hypothesis that the ratio of the two hydroxylation metabolites (2-OHE1/16alpha-OHE1) is an important risk factor for breast cancer or that it is a better predictor of breast cancer risk than levels of E1, E2 and E3 measured in urine [4].

High impact information on estrone

• E1 is also sulfated and reverted into E1S by estrogen sulfotransferase (EST) [5].
• The results indicate that E1 and E3 enhance secretion of Ag- or anti-CD3-stimulated IL-10 and IFN-gamma in dose-dependent fashion, almost identical to that of E2 [6].
• Therefore, in this study, in addition to examining the tissue distribution of both STS and EST mRNA in human adult and fetal tissues using RT followed by quantitative PCR, we studied the activity of these enzymes using (3)H-labeled E1/E1S as substrates in the homogenates of various human adult tissues [7].
• Another abnormality in endometriosis--deficient 17 beta-hydroxysteroid dehydrogenase (17 beta-HSD) type 2 expression--impairs the inactivation of estradiol (E2) to estrone (E1) [8].
• In addition, E1, but not E2, was shown to significantly decrease proliferation when added exogenously to the colonic epithelial cell line, SW620 cells [9].

Chemical compound and disease context of estrone

• After ingestion of 1 mg E2, E1 concentrations were not significantly higher in ESRD than in control subjects, peaking at 180 and 121 pg/mL, respectively (P = 0.3) [2].
• MAIN OUTCOME MEASURE(S): Urinary deoxypyridinoline (Dpyr) as marker of bone resorption and serum DHEAS, androstenedione (A-dione), testosterone (T) and estrone (E1) levels as adrenal sex steroids and their derivatives [10].
• Estrogen concentrations are very high in the leiomyoma (secretory phase, pg/g tissue [mean +/- SEM]: n = 10; E1: 147 +/- 24; E2: 850 +/- 116; E1-sulfate: 1,668 +/- 808; E2-sulfate: 718 +/- 126) [11].

Biological context of estrone

• The HA group had higher concentrations of 17PO (1.8-fold), androstenedione (1.9-fold), T (2.4-fold), and E1 (1.7-fold) than the normal group (all P < 0.001), with no alteration in circadian rhythm [12].
• Finally, the results indicate that mouse placenta is capable of converting E1 to E2 in situ, and that the synthesized E2 may be effective in a paracrine, autocrine, and/or intracrine manner and be involved in placentation [13].
• E2 levels increased rapidly after this and exceeded those of E1 until the 5th month of gestation [14].
• From that time until parturition, E1 levels equaled or exceeded those of E2 in most instances [14].
• The length of the follicular phase was significantly shorter in the group of women with the lower E1 conjugate levels [15].

Anatomical context of estrone

• 0. 16 alpha-Hydroxylation of E1S by HFL microsomes was inhibited noncompetitively by E1 [16].
• 17BetaHSD type 2, therefore, is considered to prevent the passage of excessive estrogens into the fetal circulation at endothelial cells of the intravillous fetal capillaries by catalyzing the inactivation ofE2 to E1 [17].
• The biosynthesis of estriol from E2 by fetal liver microsomes does not require an intermediate oxidation step of E2 to E1 as appears to be the case in vivo in the human adult; this was demonstrated by the formation of [17 alpha-3H]estriol from [17 alpha-3H] E2 in incubations with HFL microsomes [16].
• Aromatase, estrone (E1) sulfatase and E1 sulfotransferase activities were examined in endometrium and endometrial cancer tissue preparations [18].
• Escept for these differences, the maternal hypophysis apparently is not a major factor in the control of E1, E2 and P concentrations in pregnant rhesus monkeys [19].

Associations of estrone with other chemical compounds

• The blood samples were analyzed for radioactivity as estrone (E1), E2, their glucuronides, and E1 sulfate [20].
• Consequently, the testosterone to SHBG ratio and the E1 to A ratio were higher and the LH to FSH ratio was lower in this group [3].
• In contrast, the metabolizable C19 and C21 steroids, 5 alpha-dihydrotestosterone and 20 alpha-dihydroprogesterone, which inhibited the conversion of E1 to E2 by microsomes, stimulated E2 formation from E1 by villi [21].
• OBJECTIVE: To establish the optimum oral daily dose of micronized medroxyprogesterone acetate, given in combination with a fixed oral dose of estrone (E1) sulfate as hormone replacement therapy, that provides endometrial protection and induces cessation of vaginal bleeding [22].
• Gonadotropin-releasing hormone agonist initiated in the early follicular phase resulted in significant increases in E2, E1, and P levels compared with both midluteal or late luteal [23].

Gene context of estrone

• Kinetic analysis of semipurified hepatic ST from BKs-db/db females showed a 10-fold decrease in Km for E1 (apparent Km = 0.9 microM in mutants vs. 9.0 microM in normals) [24].
• As expected, no changes were observed in the levels of PRL and steroid hormones other than estrone (E1) and estradiol-17-beta (E2) [25].
• In the total PCO group there was a significant fall of E1 (P less than 0.05) and a decrease of E2, which reached nadirs on the third postoperative day [26].
• The conversion of 17 beta-estradiol (E2) to estrone (E1) by this enzyme can be completely inhibited in vitro by C19 and C21 steroids [21].
• Aromatase and E1 sulfatase activities in endometrial cancer tissues were found to be significantly higher than in normal endometrial tissues [18].

Analytical, diagnostic and therapeutic context of estrone

• After treating the mice with an appropriate dose of the substrate (E1, 0.1 mumol/kg.d), a marked difference in tumor growth was observed between nontransfected and HSD17B1-transfected MCF-7 cells, mean tumor weights at the end of E1 treatment being 23.2 and 130.4 mg, respectively [27].
• Furthermore, estrogen-dependent growth of the HSD17B1-expressing xenografts in the presence of E1 was markedly inhibited by administering 5 mumol/kg.d of a specific HSD17B1 inhibitor [27].
• In the second experimental series, we have examined the effects of maternal hypophysectomy on levels of E1, E2 and P either (1) in both mother and newborn baby or (2) in mother, term fetus and umbilical vein [19].
• METHODS: The extent of 17betaHSD-1, -2, -3, -4, -5, and -7 expression (measured by quantitative reverse transcriptase polymerase chain reaction) and the capacity to interconvert E1 and E2 were compared in amnion, chorion, placenta, decidua, and myometrium obtained from women at term before (n = 6) and after (n = 6) the onset of labor [28].
• Each sample was analyzed for estrone (E1), estrone sulphate (E1SO4) and estradiol-17 beta (E2) by radioimmunoassay [29].

References