PUBLICATION
Life-cycle exposure to BDE-47 results in thyroid endocrine disruption to adults and offsprings of zebrafish (Danio rerio)
- Authors
- Zhao, X., Ren, X., Ren, B., Luo, Z., Zhu, R.
- ID
- ZDB-PUB-161026-1
- Date
- 2016
- Source
- Environmental Toxicology and Pharmacology 48: 157-167 (Journal)
- Registered Authors
- Keywords
- BDE-47, Life-cycle exposure, Thyroid disruption, Zebrafish offsprings
- MeSH Terms
-
- Aging/drug effects
- Aging/metabolism*
- Animals
- Dose-Response Relationship, Drug
- Embryo, Nonmammalian/abnormalities
- Embryo, Nonmammalian/drug effects
- Embryo, Nonmammalian/metabolism
- Endocrine Disruptors/toxicity*
- Gene Expression/drug effects
- Halogenated Diphenyl Ethers/toxicity*
- Life Cycle Stages/drug effects*
- Life Cycle Stages/genetics
- Liver/drug effects
- Liver/embryology
- Liver/growth & development
- Thyroid Gland/drug effects*
- Thyroid Gland/embryology
- Thyroid Gland/growth & development
- Thyroid Gland/metabolism
- Thyroid Hormones/blood
- Thyroid Hormones/genetics
- Zebrafish/abnormalities
- Zebrafish/embryology
- Zebrafish/growth & development*
- PubMed
- 27780123 Full text @ Environ. Toxicol. Pharmacol.
Citation
Zhao, X., Ren, X., Ren, B., Luo, Z., Zhu, R. (2016) Life-cycle exposure to BDE-47 results in thyroid endocrine disruption to adults and offsprings of zebrafish (Danio rerio). Environmental Toxicology and Pharmacology. 48:157-167.
Abstract
2,2,4',4'-Tetrabromodi-phenyl ether (BDE-47) is predominantly concentrated in humans and wildlife and disturbs thyroid hormone homeostasis. The purpose of this study was to characterize the thyroid endocrine disruption induced by life-cycle exposure to BDE-47 in adults and offspring of zebrafish (Danio rerio). We exposed zebrafish embryos at the blastula stage to different concentrations of BDE-47 (1, 5, and 10μg/L). Exposure duration was 180days until fish reached adulthood. In F0 larvae, exposure decreased survival and increased malformations at 4 dpf. Thyroid hormone concentrations did not differ significantly between the F0 larvae and controls. All exposures significantly up-regulated expression of tshß, pa8, ugt1 and tg and down-regulated ttr. Significant up-regulation of dio2 and crh was observed in the 10μg/L BDE-47 group. There was no significant difference in the growth and somatic index between F0 adults and controls. BDE-47 (10μg/L) significantly decreased whole-body content of thyroxine (T4) but significantly increased triiodothyronine (T3) in both sexes. All exposures up-regulated expression of crh, tshß, pa8, ugt1 and tg and down-regulated ttr. Exposure to 10μg/L BDE-47 significantly up-regulated dio2 and ugt1 in both sexes. BDE-47 exposure (5 and 10μg/L) significantly increased the activity of pethoxy-resorufin-O-deethylase and UDP-glucuronosyl transferase. BDE-47 (10μg/L) significantly increased activity of ethoxy- and methoxy-resorufin-O-deethylase. In F1 offspring without continued BDE-47 (10μg/L) treatment, T4 significantly decreased and T3 increased. T4 was further decreased and T3 was further increased with continued BDE-47 treatment. Continued BDE-47 exposure decreased hatching and increased malformation compared with those without BDE-47 exposure. Expression of crh, tshß, dio2, pa8, ugt1 and tg was significantly up-regulated without BDE-47 exposure and with continued exposure. With continued BDE-47 exposure, dio1 was significantly up-regulated and ttr was significantly down-regulated. All the genes showed clear differences between continued exposure to 10μg/L BDE-47 and without BDE-47 exposure. These results suggest that parental exposure to BDE-47 results in thyroid endocrine disruption in adults and offspring.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping