Evidence map›Paper›PMID 21546348›Full record

ArticleToxicological sciences : an official journal of the Society of Toxicology2011

Accumulation and debromination of decabromodiphenyl ether (BDE-209) in juvenile fathead minnows (Pimephales promelas) induces thyroid disruption and liver alterations.

Pamela D Noyes, David E Hinton, Heather M Stapleton

Abstract read
In one paragraph

Article in Toxicological sciences : an official journal of the Society of Toxicology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
–field-weighted citation impact
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

28 citing papers in PubMed.

  1. Article
  2. Cross-species applicability of an adverse outcome pathway network for thyroid hormone system disruption.Toxicological sciences : an official journal of the Society of Toxicology · 2023
    Review
  3. Review
  4. Review
  5. Article
  6. Review
  7. Tissue-Based Mapping of the Fathead Minnow (Frontiers in endocrinology · 2018
    Article
  8. Article
  9. PBDE flame retardants, thyroid disease, and menopausal status in U.S. women.Environmental health : a global access science source · 2016
    Article
  10. Article
  11. Article
  12. Article
  13. Exposure of Chlamys farreri to tetrabromobisphenol A: accumulation and multibiomarker responses.Environmental science and pollution research international · 2015
    Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. Article
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.

Pamela D NoyesNicholas School of the Environment, Duke University, Durham, North Carolina 27708, USA.
David E Hinton
Heather M Stapleton

Funding

Children's Exposure to Flame Retardants: Effects on Thyroid Hormone RegulationR01ES016099 · NIEHS · DUKE UNIVERSITY · PI STAPLETON, HEATHER M · 2008 to 2017
$5.0M
NIEHS NIH HHS R01ES016099
6 · The paper itself

Abstract

Polybrominated diphenyl ether (PBDE) flame retardants are known to affect thyroid hormone (TH) regulation. The TH-regulating deiodinases have been implicated in these impacts; however, PBDE effects on the fish thyroid system are largely unknown. Moreover, the liver as a potential target of PBDE toxicity has not been explored in young fish. This study measured decabromodiphenyl ether (BDE-209) effects on TH regulation by measuring deiodinase activity in juvenile fathead minnows (Pimephales promelas). Dietary accumulations and debromination of BDE-209 were also measured, and the morphology of thyroid and liver tissues was examined. Juvenile fathead minnows (28 days old) received a 28-day dietary treatment of BDE-209 at 9.8 ± 0.16 μg/g of food at 5% of their body weight per day followed by a 14-day depuration period in which they were fed clean food. Chemical analysis revealed that BDE-209 accumulated in tissues and was metabolized to reductive products ranging from penta- to octaBDEs with 2,2',4,4',5,6'-hexabromodiphenyl ether (BDE-154) being the most accumulative metabolite. By day 28 of the exposure, rates of outer and inner ring deiodination (ORD and IRD, respectively) of thyroxine (T4) were each reduced by ∼74% among treatments. Effects on T4-ORD and T4-IRD remained significant even after the 14-day depuration period. Histological examination of treated fish showed significantly increased thyroid follicular epithelial cell heights and vacuolated hepatocyte nuclei. Enlarged biliary passageways may be the cause of the distinctive liver phenotype observed, although further testing is needed. Altogether, these results suggest that juvenile fish may be uniquely susceptible to thyroid disruptors like PBDEs.

Indexed as

AnimalsCyprinidaeDietEndocrine DisruptorsEnvironmental ExposureFlame RetardantsGlutathione TransferaseHalogenated Diphenyl EthersIodide PeroxidaseLiverThyroid GlandThyroxine2,2',4,4',5,6'-hexabromodiphenyl etherdecabromobiphenyl etherEndocrine DisruptorsFlame RetardantsGlutathione TransferaseHalogenated Diphenyl EthersIodide PeroxidaseThyroxine

Identifiers

PMID21546348
PMCPMC3155082

What OpenQuestion holds

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Registered trials

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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.