Evidence map›Paper›PMID 15811834›Full record

ArticleEnvironmental health perspectives2005

Xenoestrogens at picomolar to nanomolar concentrations trigger membrane estrogen receptor-alpha-mediated Ca2+ fluxes and prolactin release in GH3/B6 pituitary tumor cells.

Ann L Wozniak, Nataliya N Bulayeva, Cheryl S Watson

Open access · diamondAbstract readComparative Study
In one paragraph

Article in Environmental health perspectives, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 125 papers.

0numbers the graph read from it
0cells of the map it votes in
125citing papers in PubMed
11.8field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

125 citing papers in PubMed, 354 citations in OpenAlex.

  1. Advances in Research on Models of Oligoasthenozoospermia.Reproductive sciences (Thousand Oaks, Calif.) · 2026
    Review
  2. Review
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  4. Review
  5. Review
  6. Review
  7. Effect of Endocrine Disruptors on Testicular Function.Advances in experimental medicine and biology · 2025
    Review
  8. Review
  9. Effects of Endocrine-Disrupting Chemicals on Bone Health.Endocrinology and metabolism (Seoul, Korea) · 2024
    Review
  10. Article
  11. Article
  12. Endocrine Disruptor Chemicals and Children's Health.International journal of molecular sciences · 2023
    Review
  13. Article
  14. Review
  15. Review
  16. Review
  17. Article
  18. Review
  19. Review
  20. Article

65 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 1 institution in 1 country.

Ann L WozniakDepartment of Human Biological Chemistry and Genetics, University of Texas Medical Branch, Galveston, Texas 77555-0645, USA.
Nataliya N Bulayeva
Cheryl S Watson
The University of Texas Medical Branch at Galveston · US

Funding

Environmental Estrogens Acting via a Membrane ReceptorR01ES010987 · NIEHS · UNIVERSITY OF TEXAS MEDICAL BR GALVESTON · PI WATSON, CHERYL S · 2002 to 2004
$660k
NIEHS NIH HHS R01 ES010987PHS HHS 010987
6 · The paper itself

Abstract

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.

Indexed as

AnimalsBenzhydryl CompoundsBisphenol A CompoundsCalciumCell Line, TumorCoumestrolDichlorodiphenyl DichloroethyleneDieldrinDiethylstilbestrolEndosulfanEstradiolEstrogen Receptor alphaEstrogensPhenolsProlactinRatsBenzhydryl Compoundsbisphenol ABisphenol A CompoundsCalciumCoumestrolDichlorodiphenyl DichloroethyleneDieldrinDiethylstilbestrolEndosulfanEstradiolEstrogen Receptor alphaEstrogensnonylphenolPhenolsProlactinXenobiotics

Identifiers

PMID15811834
PMCPMC1278483
OpenAlexW2095582725

What OpenQuestion holds

Textmetadata
LicenceCC0
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.