Document Detail


Accumulation and debromination of decabromodiphenyl ether (BDE-209) in juvenile fathead minnows (Pimephales promelas) induces thyroid disruption and liver alterations.
MedLine Citation:
PMID:  21546348     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
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.
Authors:
Pamela D Noyes; David E Hinton; Heather M Stapleton
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.     Date:  2011-05-04
Journal Detail:
Title:  Toxicological sciences : an official journal of the Society of Toxicology     Volume:  122     ISSN:  1096-0929     ISO Abbreviation:  Toxicol. Sci.     Publication Date:  2011 Aug 
Date Detail:
Created Date:  2011-08-15     Completed Date:  2011-12-19     Revised Date:  2013-06-30    
Medline Journal Info:
Nlm Unique ID:  9805461     Medline TA:  Toxicol Sci     Country:  United States    
Other Details:
Languages:  eng     Pagination:  265-74     Citation Subset:  IM    
Affiliation:
Nicholas School of the Environment, Duke University, Durham, North Carolina 27708, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Cyprinidae / metabolism*
Diet
Endocrine Disruptors / pharmacokinetics,  toxicity
Environmental Exposure
Flame Retardants / pharmacokinetics*,  toxicity
Glutathione Transferase / analysis,  metabolism
Halogenated Diphenyl Ethers / pharmacokinetics*,  toxicity
Iodide Peroxidase / analysis,  metabolism
Liver / drug effects*,  pathology
Thyroid Gland / drug effects*,  pathology
Thyroxine / metabolism
Grant Support
ID/Acronym/Agency:
R01ES016099/ES/NIEHS NIH HHS
Chemical
Reg. No./Substance:
0/2,2',4,4',5,6'-hexabromodiphenyl ether; 0/Endocrine Disruptors; 0/Flame Retardants; 0/Halogenated Diphenyl Ethers; 1163-19-5/decabromobiphenyl ether; 7488-70-2/Thyroxine; EC 1.11.1.8/Iodide Peroxidase; EC 2.5.1.18/Glutathione Transferase
Comments/Corrections

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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