PUBLICATION
Impaired gas bladder inflation in zebrafish exposed to a novel heterocyclic brominated flame retardant tris(2,3-dibromopropyl) isocyanurate
- Authors
- Li, J., Zhang, X., Lu, J., Zhang, J., Ruan, T., Zhou, Q., Jiang, G., and Liang, Y.
- ID
- ZDB-PUB-111018-1
- Date
- 2011
- Source
- Environmental science & technology 45(22): 9750-7 (Journal)
- Registered Authors
- Keywords
- none
- MeSH Terms
-
- Zebrafish/anatomy & histology
- Zebrafish/embryology
- Zebrafish/physiology*
- Gene Expression Regulation, Developmental
- Flame Retardants/toxicity*
- Animals
- Larva/anatomy & histology
- Larva/physiology
- Triazines/toxicity*
- PubMed
- 21961643 Full text @ Env. Sci. Tech.
- CTD
- 21961643
Citation
Li, J., Zhang, X., Lu, J., Zhang, J., Ruan, T., Zhou, Q., Jiang, G., and Liang, Y. (2011) Impaired gas bladder inflation in zebrafish exposed to a novel heterocyclic brominated flame retardant tris(2,3-dibromopropyl) isocyanurate. Environmental science & technology. 45(22):9750-7.
Abstract
The teleost gas bladder is a gas-filled internal organ that processes gas exchange and controls buoyancy. Here we report that an emerging heterocyclic brominated flame retardant, tris-(2,3dibromopropyl) isocyanurate (TBC), causes defects in the inflation of the gas bladder of zebrafish larvae. This could cause impaired motility, which can ultimately lead to their death. Exposure of zebrafish embryos to TBC revealed that TBC had the most significant influence on the larvae at 72 to 96 hour post-fertilization, which coincided with the time that the gas bladder first inflats. Critical factors involved in early zebrafish gas bladder development remained at normal levels, which indicated that TBC caused defects in the inflation of the gas bladder without disrupting early organogenesis. However, the ultrastructure of the gas bladder was altered in the TBC-treated groups: the electron density of cytoplasmic vesicles was changed and the mitochondria were damaged. We deduce that TBC causes damage to mitochondria that influences the secretion of mucus-like material, resulting in defects in gas bladder inflation. For the first time, we report that the gas bladder could be a primary target organ for TBC and use of the teleost gas bladder is a new promising approach for detecting TBC toxicity.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping