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, L3
Lam, JCW2
Guo, Y3
Wu, RSS1
Lam, PKS2
Zhou, B3
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
2011 Impact Factor: 5.228
2011 SCImago Journal Rankings: 0.305
DOIhttp://dx.doi.org/10.1021/es2026592
ReferencesReferences in Scopus
DC Field
Value
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
2011 Impact Factor: 5.228
2011 SCImago Journal Rankings: 0.305
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
Author Affiliations
  1. The University of Hong Kong
  2. City University of Hong Kong
  3. Institute of Hydrobiology, Chinese Academy of Sciences