Evidence map›Paper›PMID 26999266›Full record

ArticleXenobiotica; the fate of foreign compounds in biological systems2017

Bisphenol-A glucuronidation in human liver and breast: identification of UDP-glucuronosyltransferases (UGTs) and influence of genetic polymorphisms.

Christina M Street, Zhaohui Zhu, Moshe Finel, Michael H Court

Open access · greenAbstract read
In one paragraph

Article in Xenobiotica; the fate of foreign compounds in biological systems, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
3.5field-weighted citation impact, top 9% 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

18 citing papers in PubMed, 37 citations in OpenAlex.

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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

4 authors at 2 institutions in 2 countries.

Christina M Streeta Department of Veterinary Clinical Sciences , Pharmacogenomics Laboratory, Program in Individualized Medicine (PrIMe), College of Veterinary Medicine, Washington State University , Pullman , WA , USA and.
Zhaohui Zhua Department of Veterinary Clinical Sciences , Pharmacogenomics Laboratory, Program in Individualized Medicine (PrIMe), College of Veterinary Medicine, Washington State University , Pullman , WA , USA and.
Moshe Finelb Division of Pharmaceutical Chemistry and Technology , Faculty of Pharmacy, University of Helsinki , Helsinki , Finland.
Michael H Courta Department of Veterinary Clinical Sciences , Pharmacogenomics Laboratory, Program in Individualized Medicine (PrIMe), College of Veterinary Medicine, Washington State University , Pullman , WA , USA and.
Washington State University · USUniversity of Helsinki · FI

Funding

MicroRNAs as effectors of variable human drug metabolismR01GM102130 · NIGMS · WASHINGTON STATE UNIVERSITY · PI COURT, MICHAEL H · 2012 to 2015
$1.1M
NIGMS NIH HHS R01 GM102130
6 · The paper itself

Abstract

1. Bisphenol-A is a ubiquitous environmental contaminant that is primarily metabolized by glucuronidation and associated with various human diseases including breast cancer. Here we identified UDP-glucuronosyltransferases (UGTs) and genetic polymorphisms responsible for interindividual variability in bisphenol-A glucuronidation in human liver and breast. 2. Hepatic UGTs showing the highest bisphenol-A glucuronidation activity included UGT2B15 and UGT1A9. Relative activity factor normalization indicated that UGT2B15 contributes >80% of activity at bisphenol-A concentrations under 5 μM, while UGT1A9 contributes up to 50% of activity at higher concentrations. 3. Bisphenol-A glucuronidation by liver microsomes (46 donors) ranged from 0.25 to 4.3 nmoles/min/mg protein. Two-fold higher glucuronidation (p = 0.018) was observed in UGT1A9 *22/*22 livers compared with *1/*1 and *1/*22 livers. However, no associations were observed for UGT2B15*2 or UGT1A1*28 genotypes. 4. Bisphenol-A glucuronidation by breast microsomes (15 donors) ranged from <0.2 to 56 fmoles/min/mg protein. Breast mRNA expression of UGTs capable of glucuronidating bisphenol-A was highest for UGT1A1, followed by UGT2B4, UGT1A9, UGT1A10, UGT2B7 and UGT2B15. Bisphenol-A glucuronidation was over 10-fold lower in breast tissues with the UGT1A1*28 allele compared with tissues without this allele (p = 0.006). 5. UGT2B15 and UGT1A9 contribute to glucuronidation variability in liver, while UGT1A1 is important in breast.

Indexed as

Benzhydryl CompoundsBisphenol A CompoundsBreastGlucuronosyltransferaseHazardous SubstancesHumansLiverPhenolsPolymorphism, GeneticUGT1A1 EnzymeBenzhydryl Compoundsbilirubin uridine-diphosphoglucuronosyl transferase 1A10bisphenol ABisphenol A CompoundsGlucuronosyltransferaseHazardous SubstancesPhenolsUGT1A1 EnzymeBisphenol-Abreastbreast cancerglucuronidationliver

Identifiers

PMID26999266
PMCPMC5531270
OpenAlexW2307533368

What OpenQuestion holds

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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.