Anti-Estriol polyclonal antibody

In vitro bioassays have been successfully used to screen for estrogenic activity in wastewater and surface water, however, few have been applied to treated drinking water. Here, extracts of source and treated water samples were assayed for estrogenic activity using T47D-KBluc cells and analyzed by liquid chromatography-Fourier transform mass spectrometry (LC-FTMS) for natural and synthetic estrogens (including estrone, 17 beta-estradiol, estriol, and ethinyl estradiol). None of the estrogens were detected above the LC-FTMS quantification limits in treated samples and only 5 source waters had quantifiable concentrations of estrone, whereas 3 treated samples and 16 source samples displayed in vitro estrogenicity. Estrone accounted for the majority of estrogenic activity in respective samples, however the remaining samples that displayed estrogenic activity had no quantitative detections of known estrogenic compounds by chemical analyses. Source water estrogenicity (max, 0.47 ng 17 beta-estradiol equivalents (E2Eq)L-1) was below levels that have been linked to adverse effects in fish and other aquatic organisms. Treated water estrogenicity (max, 0.078 ng E2Eq L-1) was considerably below levels that are expected to be biologically relevant to human consumers. Overall, the advantage of using in vitro techniques in addition to analytical chemical determinations was displayed by the sensitivity of the T47D-KBluc bioassay, coupled with the ability to measure cumulative effects of mixtures, specifically when unknown chemicals may be present. Published by Elsevier B.V.

The role of resveratrol (RES) in preventing breast cancer is controversial, as low concentrations may stimulate the proliferation of estrogen-receptor alpha positive (ER alpha+) breast cancer cells. As metabolism is the key factor in altering cellular estrogens, thereby influencing breast tumor growth, we investigated the effects of RES on the formation of estrogen metabolites, namely 4-androstene-3,17-dione (AD), dehydroepiandrosterone (DHEA), dehydroepiandrosterone-3-O-sulfate (DHEA-S), estrone (E1), estrone-3-sulfate (E1 -S), 17 beta-estradiol (E2), 17 beta-estradiol-3-O-(beta-D-glucuronide) (E2-G), 17 beta-estradiol-3-O-sulfate (E2-S), 16 alpha-hydroxy-17 beta-estradiol (estriol, E3), and testosterone (T) in ER alpha- MDA-MB-231 and ER alpha+ MCF-7 cells. Incubation of both of the cell lines with the hormone precursors DHEA and El revealed that sulfation and glucuronidation were preferred metabolic pathways for DHEA, E1 and E2 in MCF-7 cells, compared with in MDA-MB-231 cells, as the V-max values were significantly higher (DHEA-S: 2873.0 +/- 327.4 fmol/10(6) cells/h, E1 -S: 30.4 +/- 2.5 fmol/10(6) cells/h, E2-S: 24.7 +/- 4.9 fmol/10(6) cells/h, E2-G: 7.29 +/- 1.36 fmol/10(6) cells/h). RES therefore significantly inhibited DHEA-S, E1 -S, E2-S and E2-G formation in MCF-7, but not in MDA-MB-231 cells (K(i)s: E2-S, 0.73 +/- 0.07 mu M < E1 -S, 0.94 +/- 0.03 mu M < E2-G, 7.92 +/- 0.24 mu M < DHEA-S, 13.2 +/- 0.2 mu M). Suppression of these metabolites subsequently revealed twofold higher levels of active E2, concomitant with an almost twofold increase in MCF-7 cell proliferation, which was the most pronounced upon the addition of 5 mu M RES. As the content of RES in food is relatively low, an increased risk of breast cancer progression in women is likely to only be observed following the continuous consumption of high-dose RES supplements. Further long-term human studies simultaneously monitoring free estrogens and their conjugates are therefore highly warranted to evaluate the efficacy and safety of RES supplementation, particularly in patients diagnosed with ER alpha+ breast cancer.