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Xenoestrogen-Induced Erk-1 and Erk-2 Activation Via Multiple Membrane-Initiated Signaling Pathways

By Bulayeva, Nataliya N.

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Book Id: WPLBN0000231361
Format Type: PDF eBook
File Size: 0.2 MB
Reproduction Date: 2005

Title: Xenoestrogen-Induced Erk-1 and Erk-2 Activation Via Multiple Membrane-Initiated Signaling Pathways  
Author: Bulayeva, Nataliya N.
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Language: English
Subject: Government publications, United Nations., United Nations. Office for Disarmament Affairs
Collections: Government Library Collection, Disarmament Documents
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Publisher: United Nations- Office for Disarmament Affairs (Unoda)

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Bulayeva, N. N. (n.d.). Xenoestrogen-Induced Erk-1 and Erk-2 Activation Via Multiple Membrane-Initiated Signaling Pathways. Retrieved from http://community.schoollibrary.com/


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Government Reference Publication

Excerpt
Excerpt: Xenoestrogens can mimic or antagonize the activity of physiological estrogens, and the suggested mechanism of xenoestrogen action involves binding to estrogen receptors (ERs). However, the failure of various in vitro or in vivo assays to show strong genomic activity of xenoestrogens compared with estradiol (E2) makes it difficult to explain their ability to cause abnormalities in animal (and perhaps human) reproductive functions via this pathway of steroid action. E2 has also been shown to initiate rapid intracellular signaling, such as changes in levels of intracellular calcium, cAMP, and nitric oxide, and activations of a variety of kinases, via action at the membrane. In this study, we demonstrate that several xenoestrogens can rapidly activate extracellular-regulated kinases (ERKs) in the pituitary tumor cell line GH3/B6/F10, which expresses high levels of the membrane receptor for ER-(Alpha) (mER). We tested a phytoestrogen (coumestrol), organochlorine pesticides or their metabolites (endosulfan, dieldrin, and DDE), and detergent by-products of plastics manufacturing (p-nonylphenol and bisphenol A). These xenoestrogens (except bisphenol A) produced rapid (3?30 min after application), concentration (10?14?10?8 M)-dependent ERK-1/2 phosphorylation but with distinctly different activation patterns. To identify signaling pathways involved in ERK activation, we used specific inhibitors of ERs, epidermal growth factor receptors, Ca2+ signaling, Src and phosphoinositide-3 kinases, and a membrane structure disruption agent. Multiple inhibitors blocked ERK activation, suggesting simultaneous use of multiple pathways and complex signaling web interactions. However, inhibitors differentially affected each xenoestrogen response examined. These actions may help to explain the distinct abilities of xenoestrogens to disrupt reproductive functions at low concentrations. Key words: environmental estrogens, ERKs, estradiol, phytoestrogens, prolactinoma cell line, rapid estrogen effects.

 
 



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