Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: DrugBank:APRD00691 (EE2)
 7,802 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In vivo and in vitro studies were conducted on a male pseudohermaphrodite. Levels of gonadal steroids in peripheral blood suggested low activity of steroidogenesis which was consistent with the high levels of gonadotropins found. In vitro incubation studies with testosterone, human chorionic gonadotropin (hCG) and follicle-stimulating hormone (FSH) indicated that both gonadotropins increased the endogenous accumulation of testosterone (P less than 0.05) and the rate of conversion of testosterone to androstenedione (P less than 0.025). Estradiol accumulation was increased only in the presence of hCG. These data suggest that the aromatase and 17 beta-hydroxysteroid dehydrogenase enzyme systems in the gonads of this patient may be influenced by gonadotropins.
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PMID:An unusual case of male pseudohermaphroditism. 49 36

Plasma luteinizing hormone (LH), estradiol, progesterone, 20alpha-hydroxyprogesterone, and testosterone were radioimmunoassayed daily throughout a normal menstrual cycle, the 3rd, 6th, and 9th cycles during oral contraception with Stediril, and during stimulation with LH-releasing factor (LH-RF), human menopausal gonadotropin (HMG), and human chorionic gonadotropin (HCG). 6 women aged 23-30 took Stediril (50 mcg ethinyl estradiol and .5 mg norgestrel, combined) for 1 year. I n the control menstrual cycle, LH rose to a plateau in the follicular and luteal phases, and a high midcycle peak; estradiol rose progressively until its midcycle peak, then fell and rose again; testosterone varied with higher peaks at midcycle; progesterone began to rise on the day of the LH peak to a maximum 5-9 days after ovulation; 20alpha-hydroxyprogesterone resembled progesterone but at a lower magnit ude. During pill cycles, the subjects took 1 mg dectancyl every 6 hours starting the day before blood sampling to inhibit adrenal corticosteroids. LH, estradiol, and progesterone were very low and invariant from Days 9 to 18. 50 mcg LH-RH elicited a significant LH peak (90-370 ng/ml) within 15-30 minutes. 75 IU FSH did not stimulate formation of a corpus luteum in 3 subjects taking 4 mg dexamethasone per day, although 150 IU FSH caused a corpus luteum to develop in 1 of 3 not taking the corticosteroid. Thus LH, estradiol, and progesterone secretions were incompletely inhibited by Stediril.
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PMID:[Plasma concentrations of LH and of sex steroids during the normal menstrual cycle and during contraceptive treatment]. 76 2

Ammonium perfluorooctanoate (C8) produced an increased incidence of Leydig cell adenomas in Crl:CD BR (CD) rats fed 300 ppm for 2 years. A hormonal (nongenotoxic) mechanism was examined since C8 was negative in short-term tests for genotoxicity. Adult male CD rats were gavaged with either 0, 1, 10, 25, or 50 mg/kg C8 for 14 days. In addition, a control group was pair-fed to the 50 mg/kg C8 group. A dose-dependent decrease in body and relative accessory sex organ (ASO) weights was seen, with the relative ASO weights of the 50 mg/kg group significantly less than those of the pair-fed control. Serum estradiol levels were elevated in the 10, 25, and 50 mg/kg C8-treated animals. Estradiol levels in the 50 mg/kg C8 group were 2.7-fold greater than those in the pair-fed control. The increase in serum estradiol levels occurred at the same dose levels as the increase in hepatic beta-oxidation activity. A statistically significant downward trend with dose was seen in serum testosterone levels when compared with the ad libitum control. However, when the 50 mg/kg C8-treated rats were compared with their pair-fed control, no significant differences were seen. Challenge experiments, which can identify the presence and location of a lesion in an endocrine axis, were undertaken to clarify the significance of this downward trend in serum testosterone following C8 exposure. In the challenge experiments, adult CD rats were gavaged with either 0 or 50 mg/kg C8 for 14 days. One hour before termination, rats received either a human chorionic gonadotropin (hCG), gonadotropin-releasing hormone (GnRH), or naloxone challenge. Following hCG challenge, serum testosterone levels in the 50 mg/kg C8 were significantly decreased (50%) from those in the ad libitum controls. Similar decreases, although not significant, were seen in serum testosterone following GnRH and naloxone challenge. The challenge experiments suggest that the decrease in serum testosterone following C8 exposure is due to a lesion at the level of the testis. In addition, progesterone, 17 alpha-hydroxyprogesterone, and androstenedione were examined in the 50 mg/kg C8-treated males following hCG challenge. A 60% decrease was observed in androstenedione levels in the C8-treated animals from those in the ad libitum controls; no other differences were seen. These data suggest that the decrease in serum testosterone following hCG challenge may be due to a decrease in the conversion of 17 alpha-hydroxyprogesterone to androstenedione. The observed effects described above can be attributed to the elevated serum estradiol levels.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Induction of Leydig cell adenomas by ammonium perfluorooctanoate: a possible endocrine-related mechanism. 156 29

Patients with testicular cancer treated with cisplatin can undergo feminization that is understood poorly. Rat model studies recently showed that cisplatin can feminize in part the profile of hepatic steroid-metabolizing enzymes and circulating hormone levels. This study was undertaken to determine whether cisplatin similarly might contribute to the perturbations in gonadotropin or steroid hormone levels that can occur in patients undergoing cisplatin-based treatment for testicular cancer. Analysis of serum free testosterone, total testosterone, and androstenedione levels revealed that these hormones were not altered significantly in patients during a 38-week period of cisplatin-based treatment and follow-up. Estradiol levels were elevated before chemotherapy and were reduced to normal levels during treatment. This reduction was attributed to the cytotoxic effect of chemotherapy on the tumors and the resultant reduction in serum chorionic gonadotropin levels. Serum dihydrotestosterone (DHT) levels were normal before chemotherapy but progressively became elevated during treatment with cisplatin in five of ten patients examined. The rise in DHT may relate to the previously described increase in hepatic androgen 5 alpha-reductase activity in cisplatin-treated rats. Levels of the gonadotropins, luteinizing hormone, and follicle-stimulating hormone (FSH) were normal before cisplatin-based treatment was administered; however, FSH was elevated selectively during chemotherapy. This selective induction of FSH may reflect an effect of cisplatin on the hypothalamic secretion of gonadotropin-releasing hormone. Taken together, these findings suggest that cisplatin contributes to the perturbation of steroid and peptide hormone levels in patients with testicular cancer and perhaps in others undergoing cisplatin-based chemotherapy.
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PMID:Hormonal perturbations in patients with testicular cancer treated with cisplatin. 156 77

The effect of chronic methadone treatment upon the serum levels of Estradiol (E2), Progesterone (P), Prolactin (Prl), monkey chorionic gonadotropin (mCG), dehydroepiandrosterone sulfate (DHEAS) and Cortisol (C) in pregnant Cynomolgus monkeys (Macaca fascicularis) is described in comparison with the hormone levels in a control group. Only DHEAS was significantly decreased in late pregnancy in the methadone group. From these data it can not be concluded that methadone treatment compromises (feto)placental function. The observed intra-uterine growth retardation in the methadone treated group might be a result of a direct influence of methadone upon growth.
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PMID:The effect of chronic oral methadone treatment on monkey chorionic gonadotropin, estradiol, dehydroepiandrosterone sulfate, progesterone, prolactin and cortisol levels during pregnancy in the cynomolgus monkey (Macaca fascicularis). 182 2

To analyze the mechanisms of increased nonspecific immunity in pregnant women, the effect of various hormones on the phagocytic activity was estimated by a luminol-dependent chemiluminescence (CL) response during phagocytosing opsonized zymosan. The CL response of whole blood supplemented with exogenous human chorionic gonadotropin (hCG) increased significantly in all the male and female subjects and pregnant women. An approximate two- to fourfold increase was observed in comparison with the unsupplemented control in each subject at concentrations ranging from 1 to 1,000 IU/ml after 48 h of incubation (P less than 0.05). Progesterone slightly stimulated the CL response in female subjects only, but had no effect on male and pregnant women. Estradiol (E2) did not stimulate the CL response in any subject. The expression of Fc and C3b receptors on the surface of polymorphonuclear leucocytes (PMNL) in pregnant women was also investigated by measuring the immunofluorescence stained with monoclonal antibody to Fc and C3b receptors, respectively. The relative numbers of Fc receptors increased significantly in the third trimester compared to those of female control (P less than 0.05). Those of C3b receptor also increased in the second and third trimester (P less than 0.005). These results suggested that the nonspecific immunity represented by phagocytic activity in pregnant women increased with both oxidative metabolic responsiveness and the expression of membrane receptors. Besides, the increased phagocytic activity of the maternal host is probably due to the stimulatory effect of both endogenous and exogenous hCG on their peripheral blood phagocytes.
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PMID:Study on nonspecific immunity in pregnant women: II. Effect of hormones on chemiluminescence response of peripheral blood phagocytes. 183 54

The effects of chorionic gonadotropin (CG), estradiol, and progesterone on the cell mechanisms that determine the rate of the humoral immune response have been investigated in experiments on ovariectomized and noncastrated mice. CG (40 IU) injected into noncastrated animals increased the antibody response to sheep erythrocytes (SRBC), whereas a higher dose of the hormone (200 IU) had no effect. In contrast, both hormone doses inhibited the immune response in ovariectomized animals. Injection of estradiol (2.5 micrograms/day), but not progesterone (0.2 mg/day), into ovariectomized mice stimulated the immune response, indicating a possible role of estrogens as mediators of CG immuno-stimulating effect in noncastrated animals. Both CG does inhibited suppressor cell generation in noncastrated mice, whereas in ovariectomized animals, the hormonal effect was directly opposite. Sex steroid hormones did not influence the formation of suppressor cells. In a syngeneic transfer system, the hormones under study did not change the activity of helper T cell precursors. However, CG administration to noncastrated recipients stimulated an adoptive immune response in a dose-dependent manner. Estradiol, but not progesterone, has the same effect in ovariectomized mice. CG administration (200 IU) to ovariectomized recipients inhibited the plaque-forming cell response. This CG effect depended upon prostaglandin synthetase activity.
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PMID:Major reproduction hormones as regulators of cell-to-cell interactions in humoral immune responses. 189 18

The concentrations of the gonadotropins, luteinizing hormone (LH), and follicle-stimulating hormone (FSH) were measured in the luteal phase of the cycle in patients undergoing ovarian hyperstimulation. In nonconception cycles, FSH and LH were increased in the late luteal phase compared with conception cycles in which both gonadotropins were suppressed. Estradiol (E2) and progesterone concentrations increased in pregnancy cycles and may be the sole cause for the decreased gonadotropin concentrations as shown by equivalent concentrations of LH and FSH in both pregnancy and nonpregnancy cycles after matching for E2 concentrations. Subjects who subsequently had twin pregnancy or a spontaneous abortion were compared with those with a successful ongoing singleton conception. There were no significant differences relative to LH and FSH between the three groups, although in twin pregnancy FSH tended to be lower at day 16 from oocyte recovery. It is concluded that suppression of LH and FSH in hyperstimulated pregnancy cycles occurs after the time of the rising human chorionic gonadotropin concentrations in plasma.
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PMID:Decrease in luteal gonadotropin concentration in conception cycles after in vitro fertilization/gamete intrafallopian transfer. 189 87

A modulatory role for gonadotropin-releasing hormone (GnRH) on granulosa cell functions has been demonstrated in animals. Because human granulosa cells have specific receptors for GnRH, we have compared steroidogenesis in vitro of cells pretreated in vivo with GnRH analogs (GnRH-a) with other ovarian stimulation regimens used in in vitro fertilization (IVF) cycles. Cells from 13 patients treated with a GnRH-a for 26.8 +/- 1.1 days during pituitary desensitization and ovarian stimulation with gonadotropins were cultured. Their steroidogenesis was evaluated in basal conditions as well as after stimulation with follicle-stimulating hormone (FSH) and human chorionic gonadotropin (hCG). Granulosa-luteal cells from 9 women treated with a combination of clomiphene citrate (CC) and gonadotropins were also cultured. Estradiol production in response to FSH was stimulated only in the GnRH-a-treated cells. Basal, FSH-, and hCG-induced progesterone (P) accumulation was higher in the CC-treated cells. The peak of P production was delayed 2 days in the GnRH-a-treated group. Only cells pretreated in vivo with GnRH-a accumulated 20 alpha-hydroxyprogesterone in culture. The results of the present study suggest that the use of GnRH-a during a long period of time for IVF affects the steroidogenic pathway of human granulosa-luteal cells. It seems that, at least in part, this change is due to the stimulation of the metabolizing enzyme 20 alpha-hydroxysteroid dehydrogenase by GnRH-a.
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PMID:Steroidogenesis in vitro of human granulosa-luteal cells pretreated in vivo with gonadotropin-releasing hormone analogs. 212 84

The effect of dexamethasone (DEX) (9 alpha-Fluro-16 alpha-methyl prednisolone) on secretion of steroids by human granulosa luteinized cells was studied by culturing cells from mature follicles of women with polycystic ovarian disease and treated for infertility in the in vitro fertilization program. Patients were treated with DEX 0.5 mg/d until the day of human chorionic gonadotropin administration. The cells were cultured for 24 hours in the presence of androstenedione (10(-7)M). After incubating for 24 hours, the medium was replaced and the cells were incubated for an additional 24 hours. The medium was then harvested and assayed for estradiol (E2) and progesterone (P). Results were compared with those of a control group who was not treated with DEX. Estradiol production by cells was significantly lower in the study group treated with DEX. Progesterone production was not influenced by DEX. Follicular fluid levels, E2, and androgens did not vary with DEX treatment, whereas cortisol levels markedly decreased and P levels increased with the treatment. These findings suggest that glucocorticosteroids can directly influence granulosa luteinized cell function.
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PMID:Aromatase activity of human granulosa cells in patients with polycystic ovaries treated with dexamethasone. 220 79


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