Estrogenic receptor activity

Mn-SOD mediated by the following pathway interaction with membrane estrogen receptor, activation of MAPK, activation of NF-kB, and up-regulation of gene expression [Borras et ah, 2006 Vina et ah, 2008]. 

Molecular imaging provides novel insights on estrogen receptor activity in mouse brain. Mol Imaging. 7(6), 283-92. 

Wfe have recently carried out experiments with cell-based and animal models of inflammatory diseases. The experiments have revealed that human polymorphonuclear cells once activated with phorbol esters to cause an inflammatory response produce copious amounts of chlorinated polyphenol species. Rats treated with lipopolysaccharide (LPS) in an in vivo model of inflammatory disease heavily nitrate polyphenols in tissues (e.g., lung and liver) where inflammatory cell invasion occurs. These modified polyphenols are better antioxidants than their parent compound. Using a luciferase reporter gene assay in COS cells, both chloro- and nitrogenistein were shown to have 1-2 orders lower estrogen receptor activation than genistein itself. In summary, metabolism of polyphenols is rampant, but not always inactivating. 

Kurtev V, et al. Transcriptional regulation by the repressor of estrogen receptor activity via recruitment of histone deacetylases. 103. J. Biol. Chem. 2004 279 24834-24843. 

Chlorobenzilate did not inhibit human placental CYP 19 aromatase activity and did not express estrogen receptor activation in vitro. 

Muller RE, Teaish AM, Beebe DA and Wotiz HH (1982) Reversible inhibition of estrogen receptor activation by molybdate. J Biol Chem 257 1295 — 1300. 

An extract of Chinese rhubarb induced estrogenic activity at a concentration of 0.1 mg/ml in a yeast-based estrogen receptor activity assay (Kang et al. 2006). 

Teeguarden J. 2012. Estrogen receptor activation potential of internal concentrations of BPA in humans. Paper presented at the AAAS Meeting, February 14, 2012. Boston, MA. ... 

Pasture diarrhea, teart, molybdenosis of cattle At >3 ppm molybdenum secondary copper deficiency, dependent on copper and sulfur content of the ration Bone deformities Infertility in heifers and cows Inhibition of estrogen receptor activity in vitro Lack of libido sexualis damage of interstitial cells and germinal epithelium... 

Penttinen P, Jaehrling J, Damdimopoulos AE, et al. Diet-derived polyphenol metabolite enterolactone is a tissue-specific estrogen receptor activator. Endocrinology. 2007 148 4875-4886. 

The great variety of structures that have by now been shown to exhibit estrogenic activity leads to the suspicion that the estrogen receptor may be unusually nonspecific compared to receptors for other steroid hormones. 

Although estrone and estradiol (26) have both been isolated from human urine, it has recently been shown that it is the latter that is the active compound that binds to the so-called estrogen receptor protein. Reduction of estrone with any of a large number of reducing agents (for example, any of the complex metal hydrides) leads cleanly to estradiol. This high degree of stereoselectivity to afford the product of attack at the alpha side of the molecule is characteristic of many reactions of steroids. 

In vivo studies in animals suggest that endosulfan may disrupt normal reproductive hormone levels in male animals, but that it is not an endocrine disrupter in females. Persistent depressed testicular testosterone was seen in male rats after intermediate duration oral exposures to endosulfan. In ovariectomized female rats, orally administered endosulfan did not induce normal development of female reproductive tissues, and in female mice and immature female rats, acute parenteral exposure to endosulfan did not affect several endocrine-related end points. In vitro studies have evaluated endosulfan for estrogen receptor (ER) and cytosolic protein binding affinity, ER-mediated reporter gene expression, estrogenic induction of cell proliferation, and alteration of relative abundance of active estradiol metabolites. Overall, in vitro evidence in favor of endosulfan estrogenicity indicates relatively weak potency compared to 17[3-estradiol. Apparently contradictory results were reported in different... 

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. 

Ramamoorthy K, Wang F, Chen I-C, et al. 1997. Estrogenic activity of a dieldrin/toxaphene mixture in the mouse uterus, MCF-7 human breast cancer cells, and yeast-based estrogen receptor assays No apparent synergism. Endocrinology 138(4) 1520-1527. 

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