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At least 19 recordsLinked to original sources
PubMed1979

Lumi-mestranol and epi-lumi-mestranol.

Treatment of lumi-estrone 3-methyl ether (I) with acetylene gave the C-17-epimeric compounds lumi-mestranol (3-methoxy-17 alpha-ethynyl-13 alpha-estra-1,3,5(10)-trien-17 beta-ol, III ) and epi-lumi-mestranol (3-methoxy-17 beta-ethynyl-13 alpha-estra-1,3,5(10)-trien-17 alpha-ol, IV). The structures of the two isomers were assigned on the basis of their molecular rotations and shift-reagent experiments in the NMR. The irradiation of estrone 3-methyl ether (II) to provide compound I was investigated in two solvent systems. Minor products of these reactions were the seco-steroids VII, VIII and X.

Acetylene↗
PubMed1975

Ultrastructural effects of mestranol and norethindrone on guinea pig endometrial stromal cell.

The effect of exogenous contraceptive steroids on the ultrstructural features of the endometrial stromal cells was studied in 64 guinea pigs allotted to 4 treatment groups. Four guinea pigs from each group were killed 14, 28, 56, and 84 days after treatment with mestranol (0.01 mg/day in 1 ml of oil) or with norethindrone (0.2 mg/day in 1 ml of oil) or with a combination of both (0.001 mg of mestranol/day and 0.02 mg of norethindrone/day in 1 ml of oil) or with 1 ml of vegetable oil (oil-treated controls). An additional 12 normal guinea pigs (nontreated controls) were killed during the follicular and luteal phases of the estrous cycle, and uterine specimens were immediately collected to determine base line characteristics. During estrus, the stromal cells of these 12 guinea pigs had abundant dilated rough endoplasmic reticulum. The interstitium was filled with collagen. During the luteal phase. the cytoplasm of the stromal cells of the 12 guinea pigs contained a prominent nucleus and rough endoplasmic reticulum with undilated cisterns. The interstitium contained sparse amounts of collagen. The stromal cells of the oil-treated control guinea pigs seemed similar in ultrastructure to the stromal cells of the 12 nontreated control guinea pigs at the luteal phase. Mestranol-fed guinea pigs had dilated rough endoplasmic reticulum and well-developed Golgi apparatus within 2 weeks of initial treatment. The interstitium of mestranol-treated guinea pigs had more collagen than that of the oil-treated controls and nontreated controls during the luteal phase. Prolonged treatment with mestranol caused extensive dilation of the cisternae of the endoplasmic reticulum. The interstitium was filled with abundant collagen. Pronounced alterations in the cytoplasmic organelles or extracellular connective tissue were not ovserved in guinea pigs given norethindrone alone or norethindrone in combination with mestranol for 14 days. The stromal cells closely resembled the cells of the mature animal at luteal phase. However, the dilated rough endoplasmic reticulum that occurred in cells after mestranol treatment was not seen in stromal cells after 84 days of treatment with norethindrone. Dilation of rough endoplasmic reticulum was also observed when both the contraceptive steroids were given simultaneously for 84 days. The increased and extensively dilated rough endoplasmic reticulum seen during the follicular phase and after mestranol administration or after 84 days of treatment with mestranol and norethindrone probably indicates increased protein synthesis by the endometrial stromal cells.

Animals↗
PubMed1979

Interaction of mestranol with taurocholate uptake by isolated rat hepatocytes.

Cellular uptake interactions between mestranol and taurocholate at concentrations between 50 and 1000 microM in the medium were studied in isolated hepatocytes. Rat liver cells exposed to medium containing mestranol and taurocholate attained up to twice as large a concentration of mestranol as those exposed to mestranol without the presence of the bile acid in medium. In contrast, taurocholate concentration in cells exposed simultaneously to taurocholate and mestranol was one fourth of the concentration in cells exposed to taurocholate alone.

Animals↗
PubMed1978

Influence of 3-methylether of ethinylestradiol (Mestranol) on oviductal egg transport in rats.

The development of fertilized eggs and their transport through the oviduct were studied in rats treated orally with 3-methylether of ethinylestradiol (mestranol) at a single administration in different doses. The ED50 values were in the same range (0.11--0.34 mg mestranol/kg b.w.) as well in postcoital pregnancy inhibition test as in the experiments on tubal egg contents on day 3 as in implantation sites in niagara blue test on day 6. This suggests that the uniform cause of pregnancy inhibition of postcoital mestranol treatment on day 1 in rats is the acceleration of tubal egg transport. The ED50 of mestranol given on day 1 shortened the stay of eggs in tubes to 24 hours. Mestranol dosage above the ED50 reduced the tubal stay towards two days in comparison to five days in control animals. The number of eggs prematurely expelled from the tubes into the uterus was relatively high on day 2 and 3 in animals treated with mestranol in high dosage and with ligated cervix, compared with animals without ligation. But on day 4 on blastocysts were found. This result shows that the prevention of pregnancy is caused by the expulsion of blastocysts from uterus and/or the degeneration of zygotes in utero. Blastocysts or morulae recovered from treated rats in high dosage were transferred to the uteri of pseudopregnant recipients: 29% developed into normal term foetuses compared to 29 or 30% for both untreated control groups.

Animals↗
PubMed1976

Oral contraceptives, norethindrone and mestranol: effects on tissue levels of minerals.

The study involved three levels of dietary zinc (deficient, marginal, and adequate) and four hormonal conditions; namely, no steriods, norethindrone, mestranol, and norethindrone plus mestranol. The steroids were incorporated into diets and fed to 11-wk-old female Sprague-Dawley rats. After 10 wk of treatment, various tissues were excised for mineral assays by atomic-absorption spectrophotometry. Both steroids, reduced weight gain. Mestranol depressed plasma zinc, tibia copper and magnesium, and liver iron, but elevated the zinc levels in liver and erythrocytes, plasma copper, liver magnesium and calcium, and iron content of tibia and heart. In general, the effect was most prominent with adequate zinc but diminished in magnitude with the reduction of zinc intake. In addition, norethindrone increased heart iron and tibia calcium. Mestranol appeared to be the main causative factor and may have induced a possible shift of minerals from one pool to another. As expected, zinc deficiency resulted in the reduction of zinc concentrations of plasma, tibia, kidney, and pancreas, and the elevation of copper, iron, magnesium, and calcium concentrations of various tissues.

Animals↗
PubMed1975

Colorimetric determination of mestranol in combination with ethynodiol diacetate.

Mestranol in combination with ethynodiol diacetate, an oral contraceptive formulation, is isolated from the sample on a partition chromatographic column prior to colorimetric determination. The color reaction which is specific for estrogens is formed by shaking an aliquot of the heptane eluate of mestranol with a 30% methanol-sulfuric acid solution. A collaborative study of the method gave results of 99.8% of added mestranol for the simulated mix and 100.7% of labelled mestranol for the commercial tablet. The method has been adopted as official first aciton.

Chemical Phenomena↗
PubMed1975

Metabolism of 2-3H- and 4-14C-17alpha-ethynylestradiol 3-methyl ether (mestranol) by women.

A mixture of 2-3H and 4-14C-mestranol was administered orally to five women and 2-3H-mestranol alone to one woman. Reactions involving position 2 were extensive as judged by liberation of 3H into body water (14-45% of the dose). 17alpha-Ethynylestradiol, 2-hydroxy-17alpha-ethynylestradiol, 2-methoxy-17alpha-ethynylestradiol, 2-hydroxy-17alpha-ethynylestradiol 3-methyl ether and 16geta-hydroxy-17alpha-ethynylestradiol were measured in the "glucuronide" and pH1 fractions and mestranol, D-homoestrone-17a and D-homoestradiol-17abeta were also measured in the "glucuronide" fraction frum the urine to two of the women by reverse isotope dilution. Radioactive 2-methoxyestradiol accounted for less than 0.011% of the 14C dose in the "glucuronide" fraction of one of the women, consistent with the extent of de-ethynylation previously reported (Steroids, 25, 343 (1975).

Adult↗
PubMed1977

The influence of thiamin deficiency on the metabolism of the oral contraceptive mestranol [3-methoxy-17-ethynyl-1,3,5(10)-estratrien-17 beta-o1] by female rat liver enzymes.

Hepatic microsomes from female rats fed a thiamin deficient diet for three weeks had approximately three times the capacity to metabolize mestranol as microsomes from similar rats fed a diet rich in thiamin. The incremental addition of thiamin to the diet depressed mestranol O-demethylation, NADPH cytochrome c reductase, and cytochrome P-450 content in a dose related manner up to 2 microgram thiamin per gram of feed. Pair-feeding experiments indicate that thiamin ingestion is responsible for the depression of mestranol O-demethylation and NADPH cytochrome c reductase activity while carbodhydrate ingestion is responsible for the decrease in cytochrome P-450. The absorbance spectra generated by the binding of ethylisocyanide to microsomes yield data which suggest that there are no qualitative alterations in cytochrome P-450 due to diet.

Animals↗
PubMed1977

Influence of rifampicin treatment on the metabolic fate of [4-14C] mestranol in women.

[4-14C] Mestranol was administered to 2 rifampicin treated and to 3 untreated hysterectomised women with normal liver functions. The urinary excretions of mestranol, ethynylestradiol, 2-hydroxy-ethynylestradiol and of the total radioactivity were measured within the following 5 days. After this period the total urinary excretion of radioactivity amounted to approx. 43% (38%-50%) of the administered dose and no difference was found for the rifampicin treated and untreated women. Moreover, in the urines of both of these groups the same amounts of radioactive mestranol (1.1%-6.3% of the urinary radioactivity) and 2-hydroxy-ethynylestradiol (0.9%-3.9% of the urinary radioactivity) were measured. In contrast, the urinary excretion of ethynyl-estradiol was definitely lower in the rifampicin treated women (3.5% and 4.9% of the urinary radioactivity) as compared to the control group (15%-23%).

Adult↗
PubMed1976

Metabolism of oral contraceptive drugs. The formation and disappearance of metabolites of norethindrone and mestranol after intravenous and oral administration.

Previous studies from this laboratory reported that 3H-labeled metabolites with half-lives of more than 24 hours may remain in the plasmaa of women receiving an intravenous injection of 3H norethindrone or 3H mestranol. To confirm the presence of these metabolites, blood samples were collected for five days after injection of 3H norethindrone or 3H mestranol; 3H representing metabolites of norethindrone disappeared with half-life values of 42 to 84 hours (mean 67 hours), while 3H representing metabolites of mestranol declined with an average half-life of 45 hours (range 37 to 65 hours). When the 3H-labeled drugs were administered orally, metabolites of similar half-life were formed. Because these compounds exist for several days after a single administration and since oral contraceptive drugs are normally taken daily, the possiblity of the accumulation of 3H in the plasm of women receiving several consecutive doses of 3H norethindrone was investigated. The results of this study show a stepwise accumulation of the 3H metabolites when 3H norethindrone was administered in six daily oral doses. However, the 3H levels declined from the peak on the sixth and last day of the treatment at a rate equivalent to those previously measured after intravenous or oral administration.

Administration, Oral↗
PubMed1975

Radioimmunoassay of unconjugated plasma ethynylestradiol in women given a single oral dose of ethynylestradiol or mestranol.

A method for the radioimmunoassay of ethynylestradiol in plasma is described. The sensitivity is 18 pg/ml, recovery 86.5%, and precision 10.9% (coefficient of variation). Normal women, five at each dose level, were given 50 or 80 mug ethynylestradiol or 50, 80, or 100 mug mestranol of uniform bioavailability. Peak plasma levels were consistently obtained in the 1-hour plasma sample with the former compound. With mestranol, the peak levels of ethynylestradiol were lower than with the same quantity of ethynylestradiol and the time-curve of plasma levels much more variable. With this procedure, it is now possible to study certain aspects of the pharmacokinetics of these clinically important compounds.

Administration, Oral↗
PubMed1977

Comparison of ethinylestradiol and mestranol in sequential-type oral contraceptives in their effects on blood glucose and serum insulin in oral glucose tolerance tests.

Forty 3-hour oral glucose tolerance tests (OGTTs) were performed in 10 assumedly healthy female volunteers 19 to 30 years old, each serving four times as her own control. Each subject was taking a sequential type oral contraceptive containing either 50 microgram of ethinylestradiol or 80 microgram of mestranol alternatingly in four consecutive treatment cycles. The OGTTs were performed on the 6th day of each cycle, during pure estrogen medication. Blood glucose and serum insulin values did not differ significantly under either estrogen as tested by the t-test for paired observations. Our results do not support the findings of others that mestranol has a more pronounced or even exclusively adverse effect on glucose tolerance as compared with ethinylestradiol.

Adult↗
PubMed1975

Metabolism of 4-3-H- and 4-14-C-17alpha-ethynylestradiol 3-methyl ether (mestranol) by women.

A mixture of 4-3-H and 4-14-C-mestranol was administered orally to four women. Reactions involving position 4 were no greater than 1.7-3% of the dose as measured by liberation of 3-H into body water. The extent of de-ethynylation in vivo was no greater than 1-2% of the dose as measured by urinary estrone metabolites. Mestranol (0.7 and 0.32% of the dose), 17alpha-ethynylestradiol (6.6 and 11.3%) and 2-hydroxy-17alpha-ethynylestradiol (0.64 and 0.7%) were identified as metabolite aglycons by reverse isotope dilution after Ketodase hydrolysis of the urine from two of the women.

Administration, Oral↗
PubMed1979

The effect of menopausal status and sequential mestranol and norethisterone on serum cholesterol, triglyceride and electrophoretic lipoprotein patterns.

The serum cholesterol, triglycerides and electrophoretic lipoprotein patterns of 35 postmenopausal women, who subsequently received sequential mestranol and norethisterone, were compared with those of 35 premenopasual women of the same age and weight. The postmenopausal women had a significantly higher level of serum cholesterol (p less than 0.01) than the premenopausal women, and a significant reduction (p less than 0.001) occurred in this group after two months of therapy. There was no significant difference in level of serum cholesterol between the premenopausal group and the postmenopausal group receiving sequential mestranol and norethisterone for two months. The serum triglycerides were not significantly higher in the postmenopausal group but there was a significant increase (p less than 0.001) after two months of therapy. The marked alteration in lipid levels at the menopause may in part account for the great increase in coronary artery disease in postmenopausal women but whether these changes are reversible by giving hormone therapy remains speculative.

Adult↗
PubMed1979

Stimulatory effect of phenobarbital on the metabolism of the oral contraceptive 17 alpha-ethynylestradiol-3-methyl ether (mestranol) by rat liver microsomes.

Pretreatment of rats with phenobarbital for 4 days stimulates the activity of liver microsomal enzymes that metabolize 17 alpha-ethynylestradiol-3-methyl ether (mestranol). This effect provides an explanation for the decreased uterotropic action of mestranol in rats pretreated with phenobarbital and may provide an explanation for unwanted pregnancies in women taking oral contraceptives in combination with phenobarbital or other enzyme-inducing drugs.

Animals↗
PubMed1990

[Mestranol Reference Standard (Control 881) of National Institute of Hygienic Sciences].

The raw material of mestranol was examined for preparation of the "Mestranol Reference Standard". Analytical results for the sample were as follows: UV spectrum indicated absorption maxima at 279 and 287 nm and absorptivity at 279 nm E1%1cm 66; IR spectrum indicated specific absorption at 1612, 1578, 1505, 1253, and 1060 cm-1; optical rotation +3.9 degrees; melting point 153.1 degrees; loss on drying 0.03%; TLC and HPLC analyses indicated one impurity, respectively; the purity was assumed to be 99.3% by HPLC analysis. Based on the results, the present raw material was authorized to be the Reference Standard of the National Institute of Hygienic Sciences.

Chromatography, High Pressure Liquid↗
PubMed1976

Response of the binding capacity of plasma testosterone-estradiol-binding globulin to norethindrone, 2 mg., and mestranol, 0.1 mg., in polycystic ovarian disease.

The binding capacity of plasma testosterone-estradiol-binding globulin (TeBG) and testosterone (T) levels were measured in four women with proved polycystic ovaries and three women with a clinical diagnosis of polycystic ovarian disease before, during, and after administration of norethindrone, 2 mg., and mestranol, 0.1 mg. (N + M)...

Carrier Proteins↗
PubMed1975

Ketonitrophenols from mestranol and related compounds.

Mestranol (17alpha-ethynylestradiol 3-methyl ether), when placed on a carrier such as powdered silica gel and exposed to the atmosphere, is converted to a yellow product. The compound formed was shown to be 1alpha-ethynyltetrahydro-1beta-hydroxy4 - (2 - hydroxy - 5 - methoxy - 3 - nitrophenethyl) - 7a - methyl-5(4H)-indanone. The 3-methyl ethers of three other steroids having aromatic A rings yielded products of a similar type. Identical compounds were prepared from the respective steroids by treatment with nitrating agents in acetic acid. This reaction in acetic acid is light catalyzed. An independent synthesis of a model compound, 6-(2-hydroxy-5-methoxy-3-nitrophenyl)-3-hexanone, established the position of the constituents on the aromatic ring as well as the location of the carbonyl. The mechanism proposed for the formation of these products is an initial oxidation of the 1-substituted tetralin to form a hydroperoxide, which is ionically decomposed to form a ketophenol. The phenol is then nitrated in the ortho-position.

Acetates↗