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PubMed1988

Coregulation of C3-hydroxyl versus C17-hydroxyl glucuronidation of beta-estradiol in pregnancy and after treatment with phenobarbital or ethinyl-estradiol.

The glucuronidation of [3H]estradiol-17 beta at the C3 vs. the C17 hydroxyl groups was determined in female Sprague-Dawley rat liver microsomes. A high-performance liquid chromatography method was developed to resolve the glucuronide conjugates which were then quantitated by liquid scintillation counting. The rates of formation of 17 beta-estradiol 3-(beta-D-glucuronide) (E(2)3G) and 17 beta-estradiol 17-(beta-D-glucuronide) (E(2)17G) were 0.49 +/- 0.03 and 0.40 +/- 0.02 nmol/min/mg of protein, respectively. The apparent Km and Vmax of estradiol glucuronidation were determined in control, pregnant (day 19 of gestation), phenobarbital-treated (80 mg/kg/day i.p. for 5 days) and ethinylestradiol-treated (5 mg/kg/day i.p. for 5 days) female rats. The least-squares estimates of Km and Vmax values as well as the confidence contours of the joint sums of squares for the parameter spaces were calculated. The Vmax (nanomoles per minute per milligram of protein) for E(2)3G was significantly decreased from 0.94 to 0.57 in pregnancy and to 0.47 as a result of ethinylestradiol treatment. The Vmax values for E(2)17G were significantly different in control (0.43), pregnant (0.31) and ethinylestradiol-treated (0.27) rats. Phenobarbital treatment slightly increased the Vmax to 0.51 for E(2)17G whereas the Vmax for E(2)3G was unchanged (0.90) compared to controls. The Km (micromolar) for E(2)3G was 144 in the controls, 112 in pregnancy and 86 and 92 as a result of treatment with ethinylestradiol and phenobarbital, respectively. The Km for E(2)17G was 60 in the controls, 40 in pregnancy, 43 and 68 as a result of ethinylestradiol and phenobarbital treatment, respectively. None of the changes in Km were statistically significant.(ABSTRACT TRUNCATED AT 250 WORDS)

Algorithms↗

PubMed2000

Effects of 17 beta-estradiol and its isomer 17 alpha-estradiol on learning in rats with chronic cholinergic deficiency in the brain.

It was shown for the first time that estrogens 17 beta- and 17 alpha-estradiols compensate impaired cognitive functions in rats with partial chronic deprivation of cholinergic functions in the central nervous system induced by intracerebral administration of selective cholinergic neurotoxin AF64A. 17 beta-Estradiol produced strong dose-dependent changes in the weights of hormone-sensitive endocrine glands, while 17 alpha-estradiol did not affect the weight of the gonads and slightly influenced (in high concentration) the weights of the adrenal glands and thymus. The positive effects of exogenous 17 beta- and 17 alpha-estradiols on cognitive functions are due to their antioxidant properties, rather than due to specific action on hormone-sensitive endocrine glands.

Animals↗

PubMed1995

Synthesis of 16-(bromoalkyl)-estradiols having inhibitory effect on human placental estradiol 17 beta-hydroxysteroid dehydrogenase (17 beta-HSD type 1).

The activity of 17 beta-HSD type 1, the enzyme that converts estrone into its more potent metabolite estradiol, has been demonstrated in all classical steroidogenic tissues and almost all peripheral tissues from both rat and human. Since 17 beta-HSD is one of the most important enzymes involved in active steroid hormone formation, its inactivation could be a clinical approach to the treatment of hormono-dependent diseases like breast cancer. Herein we report the synthesis of 16-(bromoalkyl)-estradiols and their potency to inhibit the human placenta cytosolic estradiol 17 beta-HSD (type 1). Synthetic analogues possess various side chain lengths and orientation (alpha or beta) at position 16 of the steroidal D ring. The most potent inhibitory effect was observed when the length of the side chain was 3 or 4 carbons. However, the 16 beta-(bromopropyl)-estradiol easily undergoes cyclization and its effect on 17 beta-HSD is lost. Consequently, 16 alpha-(bromopropyl)-E2, 16 alpha-(bromobutyl)-E2, and 16 beta-(bromobutyl)-E2 were the best inhibitors discussed in this paper.

17-Hydroxysteroid Dehydrogenases↗

PubMed2001

A double-blind comparative study of the effects of a 23-day oral contraceptive regimen with 20 microg ethinyl estradiol and 75 microg gestodene and a 21-day regimen with 30 microg ethinyl estradiol and 75 microg gestodene on hemostatic variables, lipids, and carbohydrate metabolism.

In this double-blind study we compared the influence of two oral contraceptives, a 23-day regimen with 20 microg ethinyl estradiol and 75 microg gestodene (23-day 20/75) and a 21-day regimen with 30 microg ethinyl estradiol and 75 microg gestodene (21-day 30/75), on hemostatic variables, lipids, and carbohydrate metabolism. The volunteers received the preparations daily for six 28-day cycles. Hemostatic variables and lipids were measured at baseline and after six treatment cycles. Carbohydrate metabolism was assessed by determination of the area under the curve (AUC) of carbohydrate parameters after oral glucose tolerance tests performed at baseline and after three treatment cycles. Data from 33 volunteers in each group were obtained. No significant differences between the effects of both treatments on the hemostatic system were detected. Neither the overall change of all hemostatic variables from baseline to treatment Cycle 6 [defined as primary target variable in the study] nor the change of any of the individual hemostatic parameters differed significantly between the treatment groups. Likewise, no significant nor clinically relevant differences in the effects of both treatments on the volunteers' lipid profiles were detected. The data on carbohydrate variables suggested a slightly more favorable influence of the 23-day 20/75 regimen. The increase of the glucose AUCs after three cycles tended to be stronger with the 21-day 30/75 regimen than with the 23-day 20/75 regimen. In addition, the AUCs for insulin and C-peptide were slightly reduced after three cycles with the 23-day 20/75 regimen but slightly increased with the 21-day 30/75 regimen. Both study treatments were safe and well tolerated by the volunteers as shown by the nature and frequency of adverse events, the routine laboratory examinations, and the physical and gynecological examinations. Both preparations provided adequate contraceptive reliability. The only pregnancy during treatment was attributable to intake errors. In conclusion, the prolongation of the treatment phase of an oral contraceptives with 20 microg ethinyl estradiol does not evoke more pronounced metabolic effects than a conventional 21-day regimen with 30 microg ethinyl estradiol.

Adolescent↗

PubMed1985

Oral replacement with estradiol-cyclooctyl acetate: a new estradiol analogue. Effects on serum lipids, proteins, gonadotrophins, estrogens and uterine endometrial morphology.

Estradiol-cyclooctyl acetate (E2CoA) dissolved in arachis oil was given orally at a dose of 0.5 mg/day for 21 days to 11 oophorectomized women. The study was performed in two steps. In the first step the effects of E2CoA, administered after an overnight fast, on plasma estrone, estradiol, FSH, LH, prolactin as well as on serum proteins, fatty acids, oral glucose tolerance test and on the cervical and endometrial morphology were compared to the effects of daily oral intake of 25 micrograms ethinyl estradiol (EE) in a cross-over study. In the second step the effects of E2CoA in nonfasting conditions on plasma estrone, estradiol, FSH and LH were studied. E2CoA alleviated climacteric estrogen-deficiency symptoms in all women. It showed an estrogenic effect on cervical and endometrial morphology and depressed FSH, though more weakly than EE. No side effects were seen. The unchanged metabolic parameters after 21 days of E2CoA treatment may support the assumption of a weak estrogenic effect, but the relatively slow resorption and relatively low estradiol/estrone ratio found in this study do not confirm the hypothesis that the drug is resorbed by the chylomicrones. Further investigation on the resorption of E2CoA in nonfasting women is, however, needed.

Adult↗

PubMed2006

Estradiol and its membrane-impermeable conjugate estradiol-BSA inhibit tamoxifen-stimulated prolactin secretion in incubated rat pituitaries.

In the absence of estrogen (E), the selective E receptor modulator tamoxifen (TX) has two agonist effects in the rat pituitary: induction of progesterone receptor (PR)-dependent GnRH self-priming in the gonadotrope, and stimulation of prolactin (PRL) secretion in the lactotrope. TX-induced gonadotropin (GnRH) self-priming is absent when 10(-8) M estradiol-17beta (E2) is added to the incubation medium of pituitaries from TX-treated rats. The present experiments investigated whether PR-independent PRL release into the incubation medium of pituitaries from TX-treated ovariectomized (OVX) rats was affected by E2, and the effect of different ER ligands (ICI182780, TX, estradiol-17alpha, E2 -BSA) on TX-stimulated PRL secretion. Moreover, the effect of E2 on TRH-stimulated PRL secretion in pituitaries collected from estradiol benzoate- and TX-treated OVX rats was studied. It was found that: i) incubation with E2 supressed the PRL releasing effect of injected TX; ii) whereas coincubation with the pure anti-E type II ICI182780 antagonized the inhibitory effect of E2, coincubation with the anti-E type I TX did not; iii) estradiol-17alpha lacked inhibitory action, whereas a dose-dependent inhibitory effect of both E2 and E2 -BSA was noticed; and iv) TRH stimulatory effect on PRL release in pituitaries from TX-treated rats was blocked by addition of E2 to the medium. Taken together, these data argue in favor of the presence of specific membrane recognition sites for E in the lactotrope involved in steroid-specific E2 inhibition of TX-stimulated PRL secretion.

Animals↗

PubMed1981

Influence of 2 mg estradiol-17 beta on circulating FSH, LH, total and unconjugated estradiol levels in post-menopausal women.

The 24-hour variation in total and unconjugated serum estradiol-17 beta as well as the daily variation in one-hour serum concentration values of FSH and LH have been examined in 9 post-menopausal women given 2 mg tablets of estradiol-17 beta daily for 14 days. The tablets were manufactured according to a new dispersion method aiming at producing essentially smaller crystals, thereby enhancing the bioavailability of the estradiol-17 beta. In comparison with other preparations, this one provides a more rapid absorption, reaching peak effect after only 1 or 2 hours and presenting a higher peak than has been found with any of the others. The elimination from serum combines a rapid initial phase followed by a very slow one. Thus serum levels of estradiol-17 beta 24 hours after administration are significantly higher than the levels measured before administration of the first tablet. A rather small but significant reduction in serum LH and FSH was observed on the third and subsequent treatment days.

Aged↗

PubMed2001

Antiatherogenic effects of 17 beta-estradiol and 17 alpha-estradiol and its derivative J811 in cholesterol-fed rabbits with thyroid inhibition.

OBJECTIVE: The aim of this study was to investigate the antiatherogenic effects of 17 beta-estradiol and 17 alpha-estradiol and its derivative J811 (estra-1,3,5(10),8-tetraene-3, 17 alpha-diol), having a non-feminizing effect and high antioxidant potential, in male rabbits. EXPERIMENTAL DESIGN: Male White-Russian rabbits weighing 2.1-2.6 kg were fed either a standard or a high-cholesterol (200 mg/kg) diet, with thyroid function-inhibiting thiouracil (20 mg/kg) combined with cholic acid (40 mg/kg) administered daily in sunflower oil for 3 months. During the last month of the study, estrogens were administered by gavage at a dose of 0.02 or 0.1 mg/kg. RESULTS AND CONCLUSIONS: All three estrogens exerted remarkable antiatherosclerotic effects. Decreases in serum and aortic-wall lipid parameters and the index of atherogenicity were dependent on estrogen dose. Morphological evaluation of the aortic wall (height of plaques, size of plaque relative to aortic half-circumference) showed only weak therapeutic effects with all three estrogens. It is an open question whether the treatment period was too short to reverse the above changes. On the other hand, the data clearly suggest that 17 alpha-estradiol and J811 offer new perspectives for the prevention of atherosclerosis in men, which is similar to that found with 17 beta-estradiol in women.

Animals↗

PubMed2002

Serum estradiol and follicle-stimulating hormone levels in Thai women post total abdominal hysterectomy and bilateral oophorectomy using oral 17 beta-estradiol.

OBJECTIVE: To assess the difference of serum estradiol (E2) and follicle stimulating hormone (FSH) levels in Thai women post total abdominal hysterectomy and bilateral oophorectomy, before and after using a daily dose of 2 mg oral 17 beta-estradiol. STUDY DESIGN: Experimental study (before and after treatment). SETTING: Menopause Clinic, Department of Obstetrics and Gynecology, Faculty of Medicine, Chulalongkorn University. SUBJECTS: Thirty-five women who had undergone total abdominal hysterectomy and bilateral oophorectomy at Chulalongkorn Hospital 1 week previously due to benign gynecologic conditions were recruited in the study. Body mass index was 20-25 kg/m2. These women had no contraindication for using hormonal replacement therapy and no history of any hormonal intake in the past. INTERVENTION: All subjects were assigned to receive a daily dose of 2 mg oral 17 beta-estradiol applied at bedtime (8.00 p.m.). MAIN OUTCOME MEASURES: Serum E2 and FSH were measured before and after the study at weeks 4, 8 and 12, 12-14 hours after oral application. The hormonal measurement was performed using the time-resolved fluoroimmunoassay (FIA) method. RESULTS: Five cases were excluded, three cases due to poor compliance which was less than 85 per cent and two cases due to loss to follow-up. Of the remaining 30 cases, the mean age and body mass index were 43.03 +/- 4.58 years and 22.72 + 1.86 kg/m2, respectively. Serum E2 level significantly increased from baseline value at 4, 8 and 12 weeks (median of E2 value at 0, 4, 8 and 12 weeks: 20.00, 22.50, 324.65 and 355.35 pmol/L, p<0.001). On the other hand, there was no significant difference in the FSH serum level (median of FSH value at 0, 4, 8 and 12 weeks: 18.65, 18.40, 18.60 and 20.35 IU/L, p=0.517). CONCLUSION: A daily dose of 2 mg oral 17 beta-estradiol taken at bedtime (8.00 p.m.) for 12 weeks increased the serum E2 to the follicular phase level of the normal menstrual cycle. On the other hand, there was no significant difference in the FSH serum level.

Administration, Oral↗

PubMed2004

Variation in estradiol, estradiol precursors, and estrogen-related products in nipple aspirate fluid from normal premenopausal women.

The purpose of the study was to measure the concentrations of estradiol, its primary precursors, and factors with which it interacts in the breast, and determine their sources of variation. Nipple aspirate fluid (NAF) was collected from premenopausal women during the mid-luteal phase of the menstrual cycle. The fluid was diluted and unconjugated steroids were extracted. Estradiol was further purified by a solvent partition into aqueous NaOH. Androgens were measured in the non-phenolic fraction. Water-soluble, conjugated steroids and proteins were measured in the aqueous residue. All analytes were measured by immunoassays. Permutation methods were used to determine the correlations over multiple periods of time. The average concentration of estradiol in NAF was 435 pmol/L after purification but was many times higher when assayed without purification. Estrone and dehydroepiandrosterone (DHEA) sulfates were present in 3.7 and 75 micromol/L concentrations, respectively, while unconjugated androstenedione and DHEA were present in nanomole per liter concentrations. Lack of the steroid sulfates in NAF in 19% of subjects had no effect on NAF estradiol levels but was associated with a 77% lower concentration of unconjugated DHEA. Progesterone was present in concentrations that were 3- to 4-fold higher than normal serum concentrations (mean: 291 nmol/L). Cathepsin D, epidermal growth factor, and interleukin 6 had average values of 3.4 microg/mL, 424 ng/mL, and 1.7 ng/mL, respectively. Correlations between breasts were between 0.57 and 0.84 for the several analytes; correlations over time ranged from 0.64 and 0.93 with estrone sulfate highest in both categories. The lower correlation between breasts than within breasts indicates that local factors play an important role in determining the levels of many of these analytes in the breast. The high stability of the concentrations of several analytes over time indicates that fluctuations in environmental factors have little immediate effect on levels in the breast, and portends their utility as surrogate breast cancer risk markers.

Adult↗

PubMed2004

Serum estradiol level in Thai surgical menopausal women receiving oral micronized 17 beta-estradiol 1mg.

OBJECTIVE: To compare serum estradiol (E2) level in Thai surgical menopausal women before and after receiving a daily dose of 1 mg oral micronized 17 beta-estradiol. DESIGN: Experimental study (before and after treatment). SETTING: Gynecological ward, Hatyai regional hospital. PATIENTS: 40 premenopausal Thai women who had undergone total abdominal hysterectomy with bilateral salpingoooporectomy (Surgical menopause) for 1 week previously due to benign gynecologic conditions were recruited in the present study. These women had no contraindications for receiving hormonal replacement therapy and no history of any hormonal intake in the past. INTERVENTION: All women were assigned to receive a 1 mg micronized 17 beta-estradiol (Estrofem, Novo Nordisk A/S, Denmark) orally applied at bedtime (08.00 p.m.) each day. MEASUREMENTS: Serum estradiol (E2) levels were measured before and after treatment at 4, 8 and 12 weeks. The hormonal measurement was performed using the ELFA-technique (Enzyme Linked Fluorescent Assay). RESULTS: Four cases were excluded due to loss to follow up. Of the remaining 36 cases, the mean age (+/- SD) and the body mass index were 46.27 +/- 5. 74 years and 23.72 +/- 2.92 kg/m2, respectively. Serum E2 level significantly increased from baseline value at 4, 8 and 12 weeks (mean (+/- SD) of E2 level at 0, 4, 8 and 12 weeks: 3.82 +/- 6.30 pg/ml, 117.11 +/- 92.86 pg/ml, 135.28 +/- 91.38 pg/ml and 164.48 +/- 78.94 pg/ml, p < 0.05) respectively. CONCLUSION: A daily dose of 1 mg oral micronized 17 beta-estradiolfor 12 weeks increased the serum E2 level to the follicular phase level of the normal menstrual cycle.

Adult↗

PubMed1980

Differential lipemic and proteinemic response to oral ethinyl estradiol and parenteral estradiol cypionate.

Oral synthetic estrogen administration to normal women has been shown to result in both a lipemic and a proteinemic response. To determine whether parenteral estrogen administration would have similar results, the effects of intramuscular depo-estradiol cypionate on serum lipids and ceruloplasmin were examined. The oral and parenteral estrogens chosen for this study are frequently used therapeutically and varying doses in the range of those commonly employed clinically were given to the experimental subjects. Following oral ethinyl estradiol (20, 50, and 100 micrograms every 12 hr) comparable and significant increases in triglyceride (73 +/- 6 to 128 +/- 10 mg/dl, p < .001), ceruloplasmin (87 +/- 4 to 188 +/- 11 mg/dl, p < .001), and HDL-cholesterol (60 +/- 2 to 74 +/- 3 mg/dl, p < .001) were observed. In contrast, despite substantial increases in serum estrogens, parenteral estrogen administration (depo-estradiol cypionate, 5 and 10 mg) failed to result in alterations in any of the measured parameters. Thus, the route and/or type of estrogen administered may determine the proteinemic and lipemic effects of estrogen in man.

Administration, Oral↗

PubMed1999

Synthetic estrogen 17alpha-ethinyl estradiol induces pattern of uterine gene expression similar to endogenous estrogen 17beta-estradiol.

17alpha-Ethinyl estradiol is one of most widely prescribed estrogens. We compared the effects of this synthetic estrogen to those of the endogenous ovarian hormone 17beta-estradiol on the expression of four estrogen-inducible genes in the rat uterus. The genes examined include c-fos, c-jun, vascular endothelial growth factor, and creatine kinase B, which are all known to be primary responses to estrogen administration. Both estrogens induced the four target genes with similar time courses and produced the same pattern of cell-specific expression of c-fos and vascular endothelial growth factor in the uterine epithelium and stroma, respectively. Dose-response studies established that the potency and efficacy of both estrogens in the uterus were the same for all four hormone-regulated genes. These studies suggest that 17alpha-ethinyl and 17beta-estradiol produce similar if not identical patterns of gene expression in the uterus.

Animals↗

PubMed1992

Premature death with bladder outlet obstruction and hyperprolactinemia in New Zealand black X New Zealand white mice treated with ethinyl estradiol and 17 beta-estradiol.

OBJECTIVE: To determine causes of death, estrogen toxicity, and hyperprolactinemia in a murine model of systemic lupus erythematosus (SLE). METHODS: Female New Zealand Black x New Zealand White (NZB x NZW) mice were implanted with ethinyl estradiol, 17 beta-estradiol, or empty capsules (controls). RESULTS: Estrogen-treated mice developed striking hyperprolactinemia and died prematurely with genitourinary complications. CONCLUSION: Implanted estrogens, including 17 beta-estradiol in a dose reported previously to stimulate SLE, contribute to premature death in NZB x NZW mice, through toxic effects. Estrogen therapy increases the level of prolactin, an immunostimulatory hormone.

Animals↗

PubMed1992

The efficacy and tolerability of norgestimate/ethinyl estradiol (250 micrograms of norgestimate/35 micrograms of ethinyl estradiol): results of an open, multicenter study of 59,701 women.

The efficacy and tolerability of a new oral contraceptive, norgestimate/ethinyl estradiol (250 micrograms of norgestimate/35 micrograms of ethinyl estradiol; Cilag GmbH Research, Sulzbach, Germany) were examined in an open-label study of 59,701 women who were evaluated during 342,348 menstrual cycles; 42,022 women completed the planned treatment regimen of six cycles. A use-efficacy (overall) Pearl index of 0.25 pregnancies per 100 woman-years was calculated based on 342,348 cycles. Tolerability was assessed for all women who completed six treatment cycles. Reductions in mean cycle length and duration of bleeding were noted; 32% of the women experienced reductions in the intensity of bleeding by the end of cycle 6. After six cycles of use, amenorrhea occurred in 1%, spotting in 4%, and breakthrough bleeding in 3% of the participating women. Treatment with norgestimate/ethinyl estradiol had minimal effects on weight, blood pressure, pulse, lipid metabolism, and blood glucose. Adverse effects (acne, nausea, or headaches) occurred at low frequencies and in many cases, were reduced compared with pretreatment levels. The results of this large-scale open trial were comparable with results from two other multicenter trials of the same formulation.

Adolescent↗

PubMed1979

Estradiol 17 beta-dehydrogenase and estradiol binding in human mammary tumors.

The metabolism of estradiol was studied in 31 human breast carcinoma in vitro. All 16 estrogen-receptor-poor tumors transformed estradiol to estrone with percent conversions ranging from 11.4 to 95 except for one poorly differentiated tumor where 0.5% conversion to estrone was observed. On the contrary, only 3 out of 15 estrogen-receptor-rich tumors showed higher than 10% conversion of estradiol to estrone (p = 0.001). There is indication that the enzymatic activity in receptor-poor tumors steadily decreases in premenopausal patients as they approach menopausal age, whereas, the activity steadily increases in post-menopausal patients as the duration of menopause lengthens.

17-Hydroxysteroid Dehydrogenases↗

PubMed1989

Estradiol receptor in the lizard liver (Podarcis s. sicula). Seasonal changes and estradiol and growth hormone dependence.

This study shows that in the liver of the oviparous lizard, Podarcis s. sicula, the estrogen receptor (ER) level increases during the reproductive period (spring) when vitellogenesis occurs. This phenomenon interested both unfilled and filled ER present in the cytosolic and nuclear fractions. The increase in unfilled cytosolic and filled nuclear receptor was positively correlated to the plasma level of vitellogenin. The level of liver ER approximated that of mammalian liver ER and, therefore, it is higher than that reported for the liver of several nonmammalian species. At electrofocusing, liver ER distributes in two pH ranges (pH 6.5-7.5 and 8.0-8.8, respectively). The first form predominated in nuclei of reproductive females or of spayed estrogenized females and could represent the activated form of receptor. Ovariectomy was followed by a decrease in liver ER which can be induced in spayed females by estradiol administration. Pituitary growth hormone (GH) seemed to exert a synergic effect on estradiol liver estrogen receptor regulation. In lizards treated both with estradiol and GH, in fact, there was a significant increase in nuclear filled ER rather than an increase in the level of total nuclear ER.

Animals↗

PubMed1993

Effect of tamoxifen, estradiol 17 beta on coenzymes NAD, NADPH and the metabolism of estradiol and estrone in rabbit uterus in vivo.

Biotransformation of estradiol (E2) and estrone (E1) and the concentrations of NAD, NADPH and 17 beta-estradiol dehydrogenase (E2DH) were measured in the uterus of rabbits treated with tamoxifen (Tam) in two doses; 100 micrograms/day, (Tam 100) and 500 micrograms/day, (Tam 500), E2 (10 micrograms/day) and combination of E2 + Tam 500 for 4 days. The concentration of NAD in Tam 500 treated group was significantly higher than E2, low dose Tam and E2 + Tam 500 treated groups (P < 0.01). The concentration of NAD in E2+ Tam 500 uteri was also significantly higher than E2 treated uteri. The concentration of NADPH was not significantly different from each other amongst the various treatment groups. The studies have shown that E2DH in E2 treated uteri was less than control and Tam 500 treated groups. A significant rise in the enzyme estradiol oxidoreductase (E2OR) activity (P < 0.02) was observed in E2 + Tam 500 treated uteri over control and other treated groups whereas high dose Tam decreased the E2OR activity significantly over the E2 treated group. The rate of conversion of E1 to E2 in Tam 500 treated group was significantly less than the other treatment groups except E2 + Tam 500 treated group (P < 0.04). This study showed that E2 decreases the uterine biosynthesis of NAD and E2DH and the biotransformation of E2 to E1, while high dose Tam increases uterine NAD, E2DH activity and E2 to E1 conversion.

Animals↗