Cheryl S. Watson

TL;DR: This review is a detailed review of published studies that have focused on the mechanistic basis of BPA action in diverse experimental models and an assessment of the strength of the evidence regarding the published BPA research.

TL;DR: This document is a summary statement of the outcome from he meeting: “Bisphenol A: An Examination of the Relevance of cological, In vitro and Laboratory Animal Studies for Assessng Risks to Human Health” sponsored by both the NIEHS and IDCR at NIH/DHHS.

TL;DR: It is demonstrated that GH3/B6 rat pituitary tumor cells contain a membrane ER (mER), and confocal scanning laser microscopy of cells labeled live with the anti‐peptide antibody further supports a membrane localization of ER, suggesting that mER may be structurally similar to iER.

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: Differences between industry-funded GLP studies of BPA conducted by commercial laboratories for regulatory purposes and non-GLP studies conducted in academic and government laboratories are reviewed to identify hazards and molecular mechanisms mediating adverse effects.