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Estrogen receptors concentration

B5. Bezwoda, W. R., and Meyer, K., Effect of alpha-interferon, 17 beta estradiol, and tamoxifen on estrogen receptor concentration and cell cycle kinetics of MCF7 cells. Cancer Res. 50(17), 5387-5391 (1990). [Pg.218]

The test system was considerably less sensitive to endosulfan when mouse ER, rather than human ER, was used to mediate (3-gal activity (Ramamoorthy et al. 1997). In similar assays, endosulfan at 10 jM had no effect on (3-gal activity in yeast Saccharomyces) transfected with either the human or rainbow trout ER (Andersen et al. 1999). In addition, no effect was observed on transcriptional activation of HeLa cells transfected with plasmids containing an estrogen receptor as a responsive element (Shelby et al. 1996). Endosulfan also did not induce transient reporter gene expression in MCF-7 human breast cancer cells at an incubation concentration of 2.5 pM (Andersen et al. 1999). Maximum endosulfan-induced ER-mediated luciferase reporter gene expression occurred in vitro in a T47D human breast adenocarcinoma cell line at approximately 10 pM, while 50% expression of luciferase occurred at about 5.9 pM the maximum expression was approximately 59% of the effect from exposure to 0.03 nM estradiol (0.00003 pM) (Legler et al. 1999). Luciferase expression from combined treatment with endosulfan and dieldrin was additive over concentrations ranging from 3 to 8 pM. [Pg.171]

Toremifene is an estrogen receptor antagonist. The pharmacokinetics of toremifene are best described by a two-compartment model, with an a half-life of 4 hours and an elimination half-life of 5 days. Peak plasma concentrations are achieved approximately 3 hours after an oral dose. Toremifene is metabolized extensively, with metabolites found primarily in the feces. Toremifene is used for the treatment of metastatic breast cancer in postmenopausal women with estrogen-receptor-positive or unknown tumors. Toremifene causes hot flashes, vaginal bleeding, thromboembolism, and visual acuity changes. [Pg.1297]

PCB diets were associated with reproductive impairment including anovulation, fetal resorption, delayed ovulation, increased gestation, and decreased litter size. Hepatic estrogen binding site concentrations decreased with increasing dietary PCB concentrations but not uterine estrogen receptor sites... [Pg.1316]

Shipp, E.B., J.C. Restum, S.J. Bursian, R.J. Aulerich, and W.G. Helferich. 1998b. Multigenerational study of the effects of consumption of PCB-contaminated carp from Saginaw Bay, Lake Huron, on mink. 3. Estrogen receptor and progesterone receptor concentrations, and potential correlation with dietary PCB consumption. Jour. Toxicol. Environ. Health 54A 403-420. [Pg.1337]

Hypercoagulable states include malignancy activated protein C resistance deficiency of protein C, protein S, or antithrombin factor VIII or XI excess antiphospholipid antibodies and other situations. Estrogens and selective estrogen receptor modulators have been linked to venous thrombosis, perhaps due in part to increased serum clotting factor concentrations. Although a thrombus can form in any part of the venous circulation, the majority of thrombi begin in the lower extremities. Once formed, a venous... [Pg.176]

This book represents the effort of a group of scientists and clinicians to offer the reader an updated view of the main advances occurred in the field in the recent years. Every author has been selected because of his/her experience with modulators of estrogen receptors, either in basic or clinical grounds. This explains the structure of the book, which reviews the main basic concepts in the first part, to immediately concentrate in the recent news on the many uses of SERMs in clinical practice. We are very grateful with all of them for his excellent contribution. To conclude, we also would like to express our gratitude to Springer-Verlag for the excellent technical support as well as to those who, from different perspectives, are at the base of our work, our patients and our families. [Pg.6]

Some crucial steps in the biology of CVD have demonstrated sensitivity to estrogen agonists. Some of these actions have shown to be mediated by the classical pathway of estrogen receptors (ERs), though in other cases the involved mechanisms seem more complex and require the consideration of alternative options (Mendelsohn 2002). The available evidence concentrates on actions on lipids or on direct actions on the vascular wall. [Pg.221]

The clinical pharmacology of saw palmetto in humans is not well defined. One week of treatment in healthy volunteers failed to influence 5oo-reductase activity, DHT concentration, or testosterone concentration. Six months of treatment in patients with BPH also failed to affect prostate-specific antigen (PSA) levels, a marker that is typically reduced by enzymatic inhibition of 5ct-reductase. In contrast, other researchers have reported a reduction in epidermal growth factor, DHT levels, and antagonist activity at the nuclear estrogen receptor in the prostate after 3 months of treatment with saw palmetto in patients with BPH. [Pg.1362]


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Estrogen receptor

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