Nataliya N. Bulayeva

TL;DR: Investigation of the effects of E2 versus several XEs on the pituitary tumor cell subline GH3/B6/F10 indicates that at very low concentrations, XEs mediate membrane-initiated intracellular Ca2+ increases resulting in PRL secretion via a mechanism similar to that for E2, but with distinct patterns and potencies that could explain their abilities to disrupt endocrine functions.

TL;DR: It is demonstrated 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).

TL;DR: The authors' quantitative assays allow comparison of these outcomes for each mimetic, and let us build a detailed picture of alternative signaling pathway usage, to determine the estrogenic or antiestrogenic potential of different types of xenoestrogens, and help develop strategies for preventing xenoESTrogenic disruption of estrogen action in many tissues.

TL;DR: Many estrogen mimetic compounds are found to be potently active in the authors' quantitative extracellular-regulated kinase (ERK) activation assays, to increase cellular Ca++ levels, and to cause rapid prolactin release, however, these compounds may activate one or both mechanisms with different potencies.

TL;DR: The ability of E2 to activate ERKs in the GH3/B6/F10 pituitary tumor cell line is demonstrated and it is shown that E2 and other estrogenic compounds can produce rapid ERK phosphorylations via nongenomic pathways, using more than one pathway for signal generation.