PUBLICATION
Parental Transfer of PBDEs and Thyroid Endocrine Disruption in Zebrafish
- Authors
- Yu, L., Lam, J., Guo, Y., Wu, R., Lam, P.K., and Zhou, B.
- ID
- ZDB-PUB-111115-4
- Date
- 2011
- Source
- Environmental science & technology 45(24): 10652-9 (Journal)
- Registered Authors
- Yu, Liqun
- Keywords
- none
- MeSH Terms
-
- Animals
- Endocrine Disruptors/metabolism*
- Endocrine Disruptors/toxicity
- Female
- Flame Retardants/metabolism
- Flame Retardants/toxicity
- Halogenated Diphenyl Ethers/metabolism*
- Halogenated Diphenyl Ethers/toxicity
- Male
- Thyroid Gland/drug effects*
- Thyroid Gland/metabolism
- Water Pollutants, Chemical/metabolism*
- Water Pollutants, Chemical/toxicity
- Zebrafish
- PubMed
- 22039834 Full text @ Env. Sci. Tech.
- CTD
- 22039834
Citation
Yu, L., Lam, J., Guo, Y., Wu, R., Lam, P.K., and Zhou, B. (2011) Parental Transfer of PBDEs and Thyroid Endocrine Disruption in Zebrafish. Environmental science & technology. 45(24):10652-9.
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 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 3,5,32-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.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping