PUBLICATION
Prenatal transfer of decabromodiphenyl ether (BDE-209) results in disruption of the thyroid system and developmental toxicity in zebrafish offspring
- Authors
- Han, Z., Li, Y., Zhang, S., Song, N., Xu, H., Dang, Y., Liu, C., Giesy, J.P., Yu, H.
- ID
- ZDB-PUB-170708-1
- Date
- 2017
- Source
- Aquatic toxicology (Amsterdam, Netherlands) 190: 46-52 (Journal)
- Registered Authors
- Keywords
- BDE-209, Developmental toxicity, Hypothalamic-pituitary-thyroid axis, Thyroid endocrine disruption, Zebrafish
- MeSH Terms
-
- Animals
- Dose-Response Relationship, Drug
- Embryo, Nonmammalian/drug effects*
- Embryo, Nonmammalian/metabolism
- Embryonic Development/drug effects
- Endocrine Disruptors/analysis
- Endocrine Disruptors/toxicity*
- Female
- Halogenated Diphenyl Ethers/analysis
- Halogenated Diphenyl Ethers/toxicity*
- Male
- Receptors, Thyroid Hormone/metabolism
- Thyroid Gland/drug effects*
- Thyroid Gland/embryology
- Thyroid Gland/metabolism
- Thyroxine/metabolism
- Triiodothyronine/metabolism
- Water Pollutants, Chemical/analysis
- Water Pollutants, Chemical/toxicity*
- Zebrafish/embryology
- Zebrafish/metabolism*
- PubMed
- 28686898 Full text @ Aquat. Toxicol.
Citation
Han, Z., Li, Y., Zhang, S., Song, N., Xu, H., Dang, Y., Liu, C., Giesy, J.P., Yu, H. (2017) Prenatal transfer of decabromodiphenyl ether (BDE-209) results in disruption of the thyroid system and developmental toxicity in zebrafish offspring. Aquatic toxicology (Amsterdam, Netherlands). 190:46-52.
Abstract
Decabromodiphenyl ether (BDE-209) was one of most widely-used polybrominated diphenyl ether (PBDE) flame retardants and is frequently detected in both abiotic and biotic samples from environment. However, knowledge of its transgenerational risks is limited. Here, 4-month-old zebrafish were exposed to various concentrations of BDE-209 (0, 3, 30 or 300μg/L) for 28days and spawned in clean water without BDE-209. Concentrations of triiodothyronine (T3) and thyroxine (T4) as well as expressions of genes involved in the hypothalamic-pituitary-thyroid (HPT) axis were measured in offspring after exposure of adult zebrafish to BDE-209. BDE-209 was accumulated in adult fish and F1 eggs, which suggests transfer of this compound from adult fish to their offspring. Exposure of BDE-209 to parents resulted in developmental abnormalities in offspring and a significant decrease in T4 concentrations in F1 larvae 120h post-fertilization (hpf). Furthermore, expressions of several genes involved in the HPT axis were also altered. Expressions of thyroid hormone receptor α (tr-α), thyrotropin releasing hormone (trh), thyroid stimulating hormone β (tsh-β) and deiodinase 1 (dio 1) were significantly down-regulated in F1 individuals, while expressions of thyroid stimulating hormone receptor (tshr) and transthyretin (ttr) were significantly up-regulated. These results suggest that exposure of parent zebrafish to BDE-209 can cause developmental toxicity in offspring and disruption of the thyroid endocrine system of offspring.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping