Evidence map›Paper›PMID 20540524›Full record

ArticleChemical research in toxicology2010

Unexpected hormonal activity of a catechol equine estrogen metabolite reveals reversible glutathione conjugation.

Kuan-Wei Peng, Minsun Chang, Yue-Ting Wang, Zhican Wang, Zhihui Qin, Judy L Bolton, Gregory R J Thatcher

Abstract read
In one paragraph

Article in Chemical research in toxicology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.9field-weighted citation impact, top 22% 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

2 citing papers in PubMed, 9 citations in OpenAlex.

  1. Article
  2. Genotoxicity ofToxicology research · 2017
    Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 2 institutions in 2 countries.

Kuan-Wei PengDepartment of Medicinal Chemistry and Pharmacognosy, College of Pharmacy, University of Illinois at Chicago, 833 South Wood Street, Chicago, IL 60612-7231, USA.
Minsun Chang
Yue-Ting Wang
Zhican Wang
Zhihui Qin
Judy L Bolton
Gregory R J Thatcher
University of Illinois Chicago · USSookmyung Women's University · KR

Funding

Biotransformation of Estrogens to Carcinogenic QuinoidsR01CA073638 · NCI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI BOLTON, JUDY L. · 2001 to 2005
$1.5M
Role of electrophilic/redox active quinoids in estrogen carcinogenesisR01CA130037 · NCI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI BOLTON, JUDY L · 2007 to 2011
$1.4M
BIOTRANSFORMATION OF ESTROGEN TO CARCINOGENIC QUINOIDSR29CA073638 · NCI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI BOLTON, JUDY L. · 1997 to 2000
$107k
NCI NIH HHS CA73638NCI NIH HHS R01 CA073638NCI NIH HHS R01 CA130037NCI NIH HHS R29 CA073638
6 · The paper itself

Abstract

4-Hydroxyequilenin (4-OHEN) is a major phase I metabolite of the equine estrogens present in widely prescribed hormone replacement formulations. 4-OHEN is autoxidized to an electrophilic o-quinone that has been shown to redox cycle, generating ROS, and to covalently modify proteins and DNA and thus potentially to act as a chemical carcinogen. To establish the ability of 4-OHEN to act as a hormonal carcinogen at the estrogen receptor (ER), estrogen responsive gene expression and proliferation were studied in ER(+) breast cancer cells. Recruitment by 4-OHEN of ER to estrogen responsive elements (ERE) of DNA in MCF-7 cells was also studied and observed. 4-OHEN was a potent estrogen, with additional weak activity associated with binding to the arylhydrocarbon receptor (AhR). The potency of 4-OHEN toward classical ERalpha mediated activity was unexpected given the reported rapid autoxidation and trapping of the resultant quinone by GSH. Addition of thiols to cell cultures did not attenuate the estrogenic activity of 4-OHEN, and preformed thiol conjugates added to cell incubations only marginally reduced ERE-luciferase induction. On reaction of the 4OHEN-GSH conjugate with NADPH, 4-OHEN was observed to be regenerated at a rate dependent upon NADPH concentration, indicating that intracellular nonenzymatic and enzymatic regeneration of 4-OHEN accounts for the observed estrogenic activity of 4-OHEN. 4-OHEN is therefore capable of inducing chemical and hormonal pathways that may contribute to estrogen-dependent carcinogenesis, and trapping by cellular thiols does not provide a mechanism of termination of these pathways.

Indexed as

AnimalsCell ProliferationDNA, NeoplasmEquileninGlutathioneHorsesHumansLigandsNADPReceptors, EstrogenSulfhydryl CompoundsTumor Cells, Cultured4-hydroxy-equileninDNA, NeoplasmEquileninGlutathioneLigandsNADPReceptors, EstrogenSulfhydryl Compounds

Identifiers

PMID20540524
PMCPMC2941764
OpenAlexW2061206835

What OpenQuestion holds

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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.