The DOI matches its Crossref record; 55 of the 55 references it cites were found in a registry or an index.
Xenoestrogens at Picomolar to Nanomolar Concentrations Trigger Membrane Estrogen Receptor-α–Mediated Ca 2+ Fluxes and Prolactin Release in GH3/B6 Pituitary Tumor Cells
Open accessAbstract
Xenoestrogens (XEs) are widespread in our environment and are known to have deleterious effects in animal (and perhaps human) populations. Acting as inappropriate estrogens, XEs are thought to interfere with endogenous estrogens such as estradiol (E2) to disrupt normal estrogenic signaling. We investigated the effects of E2 versus several XEs representing organochlorine pesticides (dieldrin, endosulfan, o',p'-dichlorodiphenylethylene), plastics manufacturing by-products/detergents (nonylphenol, bisphenol A), a phytoestrogen (coumestrol), and a synthetic estrogen (diethylstilbestrol) on the pituitary tumor cell subline GH3/B6/F10, previously selected for expression of high levels of membrane estrogen receptor-alpha. Picomolar to nanomolar concentrations of both E2 and XEs caused intracellular Ca2+ changes within 30 sec of administration. Each XE produced a unique temporal pattern of Ca2+ elevation. Removing Ca2+ from the extracellular solution abolished both spontaneous and XE-induced intracellular Ca2+ changes, as did 10 microM nifedipine. This suggests that XEs mediate their actions via voltage-dependent L-type Ca2+ channels in the plasma membrane. None of the Ca2+ fluxes came from intracellular Ca2+ stores. E2 and each XE also caused unique time- and concentration-dependent patterns of prolactin (PRL) secretion that were largely complete within 3 min of administration. PRL secretion was also blocked by nifedipine, demonstrating a correlation between Ca2+ influx and PRL secretion. These data indicate that at very low concentrations, XEs mediate membrane-initiated intracellular CCa2+ 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.
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Cites
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Cited by
Hormones and endocrine-disrupting chemicals: low-dose effects and nonmonotonic dose responses
Vandenberg, L. N., Colborn, T., Hayes, T. B., Heindel, J. J., Jacobs, D. R., Lee, D.-H., Shioda, T., Soto, A. M., vom Saal, F. S., Welshons, W. V., et al. (2012) · Endocrine Reviews · doi:10.1210/er.2011-1050 · Cited by 3,209
Huang, Y. Q., Wong, C. K. C., Zheng, J. S., Bouwman, H., Barra, R., Wahlström, B., Neretin, L., & Wong, M. H. (2012) · Environment International · doi:10.1016/j.envint.2011.04.010 · Cited by 1,154
Early-life exposure to EDCs: role in childhood obesity and neurodevelopment
Braun, J. M. (2017) · Nature Reviews Endocrinology · doi:10.1038/nrendo.2016.186 · Cited by 930
In vitro molecular mechanisms of bisphenol A action.
Wetherill, Y. B., Akingbemi, B. T., Kanno, J., McLachlan, J. A., Nadal, A., Sonnenschein, C., Watson, C. S., Zoeller, R. T., & Belcher, S. M. (2007) · Reproductive Toxicology · doi:10.1016/j.reprotox.2007.05.010 · Cited by 920
Self-citationAlonso-Magdalena, P., Morimoto, S., Ripoll, C., Fuentes, E., & Nadal, A. (2006) · Environmental Health Perspectives · doi:10.1289/ehp.8451 · Cited by 632
Metadata
- Authors
- Wozniak, A. L., Bulayeva, N. N., & Watson, C. S.
- Venue
- Environmental Health Perspectives
- Publisher
- American Chemical Society (ACS)
- Published
- 2005-04
- Volume
- 113
- Issue
- 4
- Pages
- 431-439
- ISSN
- 0091-6765 (ISSN-L)
- 1552-9924
- OpenAlex
- W2095582725
- Cited by
- 358
- References
- 55
- FWCI
- 15.07
- Type
- journal article
- Language
- en
- Open access
- gold
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- Wozniak, A. L., Bulayeva, N. N., & Watson, C. S. (2005). Xenoestrogens at Picomolar to Nanomolar Concentrations Trigger Membrane Estrogen Receptor-α–Mediated Ca 2+ Fluxes and Prolactin Release in GH3/B6 Pituitary Tumor Cells. Environmental Health Perspectives. https://doi.org/10.1289/ehp.7505
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