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Article: Parental transfer of polybrominated diphenyl ethers (PBDEs) and thyroid endocrine disruption in zebrafish
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TitleParental transfer of polybrominated diphenyl ethers (PBDEs) and thyroid endocrine disruption in zebrafish
 
AuthorsYu, L2
Lam, JCW3
Guo, Y2
Wu, RSS1
Lam, PKS3
Zhou, B2
 
Issue Date2011
 
PublisherAmerican Chemical Society. The Journal's web site is located at http://pubs.acs.org/est
 
CitationEnvironmental Science And Technology, 2011, v. 45 n. 24, p. 10652-10659 [How to Cite?]
DOI: http://dx.doi.org/10.1021/es2026592
 
AbstractPolybrominated diphenyl ethers (PBDEs) have the potential to disrupt the thyroid endocrine system. The objective of the present study was to characterize the disrupting effects of long-term exposure on the thyroid endocrine system in adult fish and their progeny following parental exposure to PBDEs. Zebrafish (Danio rerio) embryos were exposed to environmentally relevant concentrations (1, 3, and 10 μg/L) of the PBDE mixture DE-71 for 5 months until sexual maturation. In the F0 generation, exposure to DE-71 significantly increased plasma thyroxine (T4) but not 3,5,3′-triiodothyronine (T3) in females. This increased T4 was accompanied by decreased mRNA levels of corticotropin-releasing hormone (CRH) and thyrotropin β-subunit (TSHβ) in the brain. The F1 generation was further examined with or without continued DE-71 treatment conditions. Exposure to DE-71 in the F0 fish caused significant increases in T4 and T3 levels in the F1 larvae and modified gene expressions in the hypothalamic-pituitary-thyroid axis (HPT axis) under both conditions. Decreased hatching and inhibition of growth in the F1 offspring were observed in the condition without DE-71 treatment. Continued DE-71 treatment in the F1 embryos/larvae resulted in further decreased hatching, and increased malformation rates compared with those without DE-71 exposure. Analysis of F1 eggs indicated that parental exposure to DE-71 could result in a transfer of PBDEs and thyroid hormones (THs) to their offspring. For the first time, we demonstrated that parental exposure to low concentrations of PBDEs could affect THs in the offspring and the transgenerational PBDE-induced toxicity in subsequent nonexposed generations. © 2011 American Chemical Society.
 
ISSN0013-936X
2013 Impact Factor: 5.481
 
DOIhttp://dx.doi.org/10.1021/es2026592
 
ReferencesReferences in Scopus
 
DC FieldValue
dc.contributor.authorYu, L
 
dc.contributor.authorLam, JCW
 
dc.contributor.authorGuo, Y
 
dc.contributor.authorWu, RSS
 
dc.contributor.authorLam, PKS
 
dc.contributor.authorZhou, B
 
dc.date.accessioned2012-09-20T08:25:45Z
 
dc.date.available2012-09-20T08:25:45Z
 
dc.date.issued2011
 
dc.description.abstractPolybrominated diphenyl ethers (PBDEs) have the potential to disrupt the thyroid endocrine system. The objective of the present study was to characterize the disrupting effects of long-term exposure on the thyroid endocrine system in adult fish and their progeny following parental exposure to PBDEs. Zebrafish (Danio rerio) embryos were exposed to environmentally relevant concentrations (1, 3, and 10 μg/L) of the PBDE mixture DE-71 for 5 months until sexual maturation. In the F0 generation, exposure to DE-71 significantly increased plasma thyroxine (T4) but not 3,5,3′-triiodothyronine (T3) in females. This increased T4 was accompanied by decreased mRNA levels of corticotropin-releasing hormone (CRH) and thyrotropin β-subunit (TSHβ) in the brain. The F1 generation was further examined with or without continued DE-71 treatment conditions. Exposure to DE-71 in the F0 fish caused significant increases in T4 and T3 levels in the F1 larvae and modified gene expressions in the hypothalamic-pituitary-thyroid axis (HPT axis) under both conditions. Decreased hatching and inhibition of growth in the F1 offspring were observed in the condition without DE-71 treatment. Continued DE-71 treatment in the F1 embryos/larvae resulted in further decreased hatching, and increased malformation rates compared with those without DE-71 exposure. Analysis of F1 eggs indicated that parental exposure to DE-71 could result in a transfer of PBDEs and thyroid hormones (THs) to their offspring. For the first time, we demonstrated that parental exposure to low concentrations of PBDEs could affect THs in the offspring and the transgenerational PBDE-induced toxicity in subsequent nonexposed generations. © 2011 American Chemical Society.
 
dc.description.natureLink_to_subscribed_fulltext
 
dc.identifier.citationEnvironmental Science And Technology, 2011, v. 45 n. 24, p. 10652-10659 [How to Cite?]
DOI: http://dx.doi.org/10.1021/es2026592
 
dc.identifier.doihttp://dx.doi.org/10.1021/es2026592
 
dc.identifier.epage10659
 
dc.identifier.hkuros208936
 
dc.identifier.hkuros203339
 
dc.identifier.issn0013-936X
2013 Impact Factor: 5.481
 
dc.identifier.issue24
 
dc.identifier.pmid22039834
 
dc.identifier.scopuseid_2-s2.0-83455187174
 
dc.identifier.spage10652
 
dc.identifier.urihttp://hdl.handle.net/10722/165949
 
dc.identifier.volume45
 
dc.languageeng
 
dc.publisherAmerican Chemical Society. The Journal's web site is located at http://pubs.acs.org/est
 
dc.publisher.placeUnited States
 
dc.relation.ispartofEnvironmental Science and Technology
 
dc.relation.referencesReferences in Scopus
 
dc.titleParental transfer of polybrominated diphenyl ethers (PBDEs) and thyroid endocrine disruption in zebrafish
 
dc.typeArticle
 
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<description.abstract>Polybrominated diphenyl ethers (PBDEs) have the potential to disrupt the thyroid endocrine system. The objective of the present study was to characterize the disrupting effects of long-term exposure on the thyroid endocrine system in adult fish and their progeny following parental exposure to PBDEs. Zebrafish (Danio rerio) embryos were exposed to environmentally relevant concentrations (1, 3, and 10 &#956;g/L) of the PBDE mixture DE-71 for 5 months until sexual maturation. In the F0 generation, exposure to DE-71 significantly increased plasma thyroxine (T4) but not 3,5,3&#8242;-triiodothyronine (T3) in females. This increased T4 was accompanied by decreased mRNA levels of corticotropin-releasing hormone (CRH) and thyrotropin &#946;-subunit (TSH&#946;) in the brain. The F1 generation was further examined with or without continued DE-71 treatment conditions. Exposure to DE-71 in the F0 fish caused significant increases in T4 and T3 levels in the F1 larvae and modified gene expressions in the hypothalamic-pituitary-thyroid axis (HPT axis) under both conditions. Decreased hatching and inhibition of growth in the F1 offspring were observed in the condition without DE-71 treatment. Continued DE-71 treatment in the F1 embryos/larvae resulted in further decreased hatching, and increased malformation rates compared with those without DE-71 exposure. Analysis of F1 eggs indicated that parental exposure to DE-71 could result in a transfer of PBDEs and thyroid hormones (THs) to their offspring. For the first time, we demonstrated that parental exposure to low concentrations of PBDEs could affect THs in the offspring and the transgenerational PBDE-induced toxicity in subsequent nonexposed generations. &#169; 2011 American Chemical Society.</description.abstract>
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Author Affiliations
  1. The University of Hong Kong
  2. Institute of Hydrobiology, Chinese Academy of Sciences
  3. City University of Hong Kong