ArticleEnvironmental health perspectives2008
Styrene trimer may increase thyroid hormone levels via down-regulation of the aryl hydrocarbon receptor (AhR) target gene UDP-glucuronosyltransferase.
Article in Environmental health perspectives, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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7 citing papers in PubMed, 36 citations in OpenAlex.
- Oligomeric lactic acid nanoplastics induce intrauterine growth restriction in mice by disrupting GATA2-mediated placental vascular development.PLoS biology · 2026Article
- Acute styrene exposure induces hepatocellular injury and molecular stress responses inVeterinary world · 2025Article
- Oligomers from the Synthetic Polymers: Another Potential Iceberg of New Pollutants.Environment & health (Washington, D.C.) · 2023Review
- Migration of styrene oligomers from food contact materials: in silico prediction of possible genotoxicity.Archives of toxicology · 2022Article
- Article
- Upregulation of Ugt1a genes in placentas and fetal livers in a murine model of assisted reproduction.Placenta · 2012Article
- Use of transgenic mice in UDP-glucuronosyltransferase (UGT) studies.Drug metabolism reviews · 2010Article
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Authors and funding
11 authors at 5 institutions in 2 countries.
Funding
Abstract
backgroundStyrene trimers (STs) are polystyrene-container-eluted materials that are sometimes detected in packaged foods. Although the possible endocrine-disrupting effects of STs, such as estrogenic activities, have been reported, their potential thyroid toxicity, such as that caused by the related endocrine disruptor 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), has not been studied in detail.
objectiveUsing wild-type and aryl hydrocarbon receptor (Ahr)-null mice, we investigated whether 2,4,6-triphenyl-1-hexene (ST-1), an isomer of STs, influences thyroxin (T(4)) levels in the same manner as TCDD, which induces UDP-glucuronosyltransferase (UGT) via the AhR, resulting in a decrease in T(4) levels in the plasma of mice.
methodsBoth wild-type and Ahr-null mice (five mice per group) were treated for 4 days by gavage with ST-1 (0, 32, or 64 micromol/kg).
resultsHigh-dose (64 micromol/kg) ST-1 decreased the expression of AhR, cytochrome P450 (CYP) 1A1/2, UGT1A1/A6, and CYP2B10 mRNAs and the enzyme activity for CYP1A and UGT1A only in the wild-type mice. This dose decreased AhR DNA binding, but paradoxically increased AhR translocation to the nucleus. In contrast, a high dose of ST-1 increased T(4) levels in the plasma in wild-type mice but did not influence T(4) levels in AhR-null mice.
conclusionsAlthough ST-1 treatment might cause an increase in AhR levels in the nucleus by inhibiting AhR export, this chemical down-regulated AhR mRNA, thus leading to down-regulation of AhR target genes and an increase in plasma T(4) levels.
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