Effects Of Synthetic Estrogens Research Articles

The Effect of Synthetic Estrogens on Fathead Minnow Populations

The fathead minnow (Pimephales promelas) is a freshwater fish with a wide distribution in lakes, streams, and ponds across North America, including Ontario. This species has been recognized as one of the most useful model organisms for freshwater toxicology monitoring, due to its tolerance of its range for aquatic conditions. Synthetic estrogens are excreted as a metabolic product in the urinary waste of women using oral contraceptives. Estrogens are not effectively filtered out by sewage treatment plants and are subsequently released into water effluents, affecting aquatic wildlife. In response to experimentally heightened estrogen concentrations, male and female fathead minnows have shown increases in vitellogenin protein, and females have displayed delayed ovarian development and increased numbers of underdeveloped ovarian follicles. Males also experienced lowered gonadosmatic indices, and some males had primary stage oocytes in their testes. As would be expected, synthetic estrogen additions influenced fathead minnow reproductive success, leading to a collapse of the experimental fish population. By taking a multi-disciplinary approach, this study looks to identify how synthetic estrogens are threatening local fish populations, and how this may eventually disrupt the freshwater food chain. Collaboration with The Canadian Association on Water Quality (Kingston), Ravensview Wastewater Treatment Plant, and the Catarqui Region Conservation Authority will provide a greater understanding of the hormonal content in Kingston’s wastewaters. Ultimately, this study will provide more insight on the level of risk faced by freshwater fish populations on a local scale, and propose a method to reduce estrogen deposition in freshwater environments.

Вплив синтетичних естрогенів на показники прооксидантно-антиоксидантної системи органів щурів різного віку в дослідах in vitro

Вплив синтетичних естрогенів на показники прооксидантно-антиоксидантної системи органів щурів різного віку в дослідах in vitro

Estrogen receptor-mediated transcriptional activation by 17 beta-estradiol and its analogs.

We investigated the effects of natural and synthetic estrogens on estrogen receptor-mediated signal transduction and transcription. To assess estrogen receptor-dependent gene expression, we constructed a reporter plasmid that can express the luciferase gene under the control of the estrogen-responsive element. A transcriptional assay was performed by transfection of the reporter plasmid into estrogen-responsive MCF-7 cells. Transcription was completely dependent on the natural estrogen, 17 beta-estradiol (E2), in a dose-dependent manner. Retinoic acids and other steroid hormones had no effect on gene expression. The effect of synthetic estrogens on estrogen receptor-mediated signal transduction was also examined using the specific reporter assay system. A synthetic estrogen, diethylstilbestrol, exhibited higher activity than E2 at lower concentrations. In addition, transcriptional activities of the (+)- and (-)-enantiomers of indenestrol A, a metabolite of diethylstilbestrol, could be distinguished using the reporter assay system.

Effect of synthetic estrogen on platelet aggregation and vascular release of PGI 2-like material in the rabbit

Treatment of adult female New Zealand white rabbits with ethinyl estradiol, the synthetic estrogen used in many oral contraceptives, results in a significant increase in in vivo aggregation. This alteration in platelet behavior is accompanied by diminished vascular release of antiaggregatory PGI 2 (prostacyclin)-like material. Addition of a progestin prevents the change in platelet aggregation seen with the estrogen alone. Diminished vascular PGI 2 release may be an important factor in the pathogenesis of thrombotic occurrences experienced by some oral contraceptive users. In vivo platelet aggregation may be of value in identifying individuals at risk of developing thrombotic disturbances while taking oral contraceptives.

Behavioral effects of ethynyl estrogens in the female rat

The synthetic analogues of estradiol, ethynyl estradiol and mestranol, are used in oral contraceptives. Their effects on food intake and sexual behavior were evaluated in female rats, and compared with those of estradiol. It was found (Experiment 1) that both ethynyl estradiol and mestranol reduced food intake reliably, and more than estradiol. Water intake and body weight followed similar trends. Ethynyl estradiol, but not mestranol, plus progesterone stimulated proceptive and receptive behavior in ovariectomized female rats. Daily administration of ethynyl estrogens without progesterone showed similar trends (Experiment 3). It is hoped that these studies provide guidelines for further work on the effects of synthetic estrogens on sub-primate and primate behavior.

Role of oral contraceptive agents in the pathogenesis of liver tumors

Since the introduction of oral contraceptive steroids in 1960 there has been a sharp increase in the incidence of benign liver tumors. Epidemiologic and other evidence links focal nodular hyperplasia and hepatic cell adenoma to the use of these agents. The risk increases with long-term exposure. The majority of patients were less than 35 years old. Most patients were exposed to mestranol (ME) alone or alternately with ethinylestradiol, both synthetic steroidal estrogens. Inability to demethylate ME in the smooth endoplasmic reticulum of hepatocytes may allow massive accumulation of oncogenic metabolites. This is probably a pharmacogenetic variable in a small number of women. Cholestasis, hypervascularity, induction of intracellular enzyme systems, thrombogenesis, and thickening of arterial and venous walls are other known effects of synthetic estrogens and progestogens. All may contribute to the pathogenesis of liver tumors. Many patients are asymptomatic until there is rapid expansion of the tumor. Pain occurs when Glisson's capsule stretches. Intrahepatic bleeding and liver rupture are common sequelae. Ligation of the hepatic artery may be lifesaving in the face of exsanguinating liver bleeding. Reports of regression with observation alone are encouraging. Instances of progression of unresected adenomas to rupture during subsequent pregnancy dictate avoidance of sex steroids in patients with hepatic neoplasia. Sonography, computerized axial tomography, radionuclide scans, and selective celiohepatic angiography are useful methods for the diagnosis of liver tumor in the symptomatic patient. There is a primary need to develop biochemical methods for detecting patients at risk for developing liver tumors. Epidemiologic research and central reporting of case histories are needed in the search for common factors.

Effect of synthetic estrogens and estrogen-progestin combinations on the hepatic microsomal enzyme system

Pretreatment of male rats with mestranol or ethynyl estradiol 10 min prior to the administration of pentobarbital had no effect on the duration of pentobarbital-induced sleep. Although the estrogens are alternate substrates for the microsomal enzyme system which metabolizes pentobarbital, the concentrations used in this study did not affect pentobarbital metabolism. Chronic pretreatment with mestranol or ethynyl estradiol did not induce the hepatic microsomal enzyme system, as determined by measuring the concentration of cytochrome P-450, the rate of activity of cytochrome P-450 reductase and the amount of microsomal protein/g of rat liver. However, chronic pretreatment with ethynyl estradiol or mestranol markedly decreased the daily body weight gain of the rats, but did not significantly alter the weight of their livers.

The effects of synthetic estrogens on the metabolic clearance and production rates of estrone and estradiol

The metabolic clearance rates (MCR) of estrone (1) and estradiol were determined by pulse injections and constant infusions of 3H-estrone and 3H-estradiol in seven women taking mestranol-containing compounds and in seven women taking ethinyl estradiol-containing compounds. These results were compared with the results previously obtained in our laboratory (2, 3, 4, 5) in comparable women not taking these compounds. In the women taking mestranol the mean (± SE) MCR for estradiol, 750 ± 600 1/day/m 2, was similar to our normal mean value, 790 ± 30 1/day/m 2. However, the mean MCR for estrone was less 1,010 ± 60 1/day/m 2 than that in normals 1,230 ± 30 1/day/m 2. In the women taking ethinyl estradiol the mean MCR for estradiol, 1,070 ± 60 1/day/m 2 was significantly ( P < 0.01) greater than the normal value. The mean MCR for estrone, 1,180 ± 80 1/day/m 2 was not different from the normal. Using an immunoassay to measure the concentrations of estradlol and. estrone in plasma, the mean level of estradlol in mestranol users was 40 ± 7 Pg/ml and in ethinyl estradlol users 69 ± 4 pg/ml. The mean calculated production rate for estradlol in the mestranol users was 47 ± 8 μg/day and in the ethinyl estradlol users was 120 ± 22 μg/day. The mean calculated, production rates for estrone were 71 ± 12 and 93 ± 12 μg/day in the respective groups. Thus while mestranol appears to have little effect on endogenous estrogen metabolism, the use of ethinyl estradiol appears to increase the MCR of estradlol, but not of estrone. The MCR of estradlol returns to the normal range when ethinyl estradlol is stopped.

Exogenous hormones in pregnancy.

Various changes that have been observed after intrauterine exposure to exogenous hormones are presented. Often, alterations observed after exogenous maternal hormone therapy consist of varying degrees of masculinization of the female genitalia. The following specific drug interactions are described in some detail: 1) effects of progestational agents and androgens on female genitalia; 2) relationship of corticosteroids to the development of cleft palate; and 3) effects of synthetic estrogens (e.g., diethylstilbestrol) on the female reproductive tract. The discussion closes with a review of the association of therapy with such drugs to the delayed appearance of clear-cell adenocarcinoma of the genital tract in young women.

合成発情物質の埋没がめん羊の蛋白質代謝におよぼす影響

合成発情物質の埋没がめん羊の蛋白質代謝におよぼす影響

The Effects of Synthetic Estrogens on Energy Metabolism in Chicks

The effects of synthetic estrogens on energy metabolism in chicks were studied. The results obtained were as follows.1. The body weight gain of the treated chicks was higher than that of the control in one case, but in most cases the differences were not statistically significant.2. The increases in cholesterol and lipid contents of the blood, liver, abdominal and tissue fat might be stored in tissues, thus making the chicks fatter.3. The metabolizable energy of the diet was the same for both the control and synthetic estrogen treated lots. The productive energy of the diet was numerically in favor of the control lots. These results indicated that estrogen treatment did not improve digestibility and net energy yield, neither did it lower heat production.4. Protein gain in chicks was reduced by estrogen treatment.5. Fat was being deposited following estrogen supply, less total gain per unit of metabolizable energy consumed was observed because of the relatively high caloric concentration of adipose tissue.6. The increase in the amount of fat deposited appears to be due to the increased feed intake per unit of weight gain.

EFFECT OF SYNTHETIC ESTROGENS ON NAD(P) TRANSHYDROGENASE OF RAT PLACENTA.

EFFECT OF SYNTHETIC ESTROGENS ON NAD(P) TRANSHYDROGENASE OF RAT PLACENTA.

The Effect of Season and Estrogenic Hormones on Market Grade of Chickens

THE effect of synthetic estrogens on market finish, weight gain and feed efficiency is well known. Diethylstilbestrol pellets or dienestrol diacetate in the feed improves market grade, as shown by Begin and Grainger (1957), Detwiler, Andrews and Bohren (1950), Hebert and Brunson (1957), Matterson, Potter and Singsen (1959), Boone and Morgan (1961), Lorenz (1945), and Andrews and Bohren (1957). Diethlystilbestrol has been incorporated into the feed by Sykes, Davidson and Barrett (1945), Lorenz (1945) and Glazener and Jull (1946). Feed efficiency was found to be the same as the controls or improved by the addition of the hormone in all of the above cases with the exception of Begin and Grainger (1957) and Hebert and Brunson (1957). In most of the above cases the rate of gain was also increased or improved by the use of the estrogen. The effect of season is not so well known. Goodale (1926)…

A Comparison of the Gains 5 in Weight, Fat Deposition and Market Quality of Estrogen-Treated Cockerels and Capons

The effects of synthetic estrogens upon the fattening and market quality of chickens of different ages have been reported by Black and Booth (1946), Jaap and Thayer (1944), Lorenz (1945), Thayer, Jaap and Penquite (1945), Sykes, Davidson and Barrett (1945), and others. These investigators have shown that the meat quality of birds thus treated is improved over that of untreated birds, but the degree of improvement, in most cases, is difficult to evaluate.Poultrymen have made inquiries as to how estrogen-treated males compared with capons in meat quality and whether or not such treatments would supplant caponizing in the production of superior meat birds.In an attempt to answer this question, comparative studies were made of the gains in weight, fat deposition, market quality and eating quality of the meat of estrogenized cockerels, untreated cockerels, and capons.Rhode Island Red males from 7½ to 8½ months of age were injected .