PUBLICATION

Multiple bio-analytical methods to reveal possible molecular mechanisms of developmental toxicity in zebrafish embryos/larvae exposed to tris(2-butoxyethyl) phosphate

Authors
Han, Z., Wang, Q., Fu, J., Chen, H., Zhao, Y., Zhou, B., Gong, Z., Wei, S., Li, J., Liu, H., Zhang, X., Liu, C., Yu, H.
ID
ZDB-PUB-140513-242
Date
2014
Source
Aquatic toxicology (Amsterdam, Netherlands)   150: 175-81 (Journal)
Registered Authors
Gong, Zhiyuan, Li, Jun
Keywords
Developmental toxicity, Flame retardants, TBEP, Zebrafish, iTRAQ
MeSH Terms
  • Animals
  • Apoptosis/drug effects
  • Fish Proteins/genetics
  • Gene Expression Profiling
  • Gene Expression Regulation/drug effects
  • Organophosphorus Compounds/pharmacokinetics
  • Organophosphorus Compounds/toxicity*
  • Water Pollutants, Chemical/pharmacokinetics
  • Water Pollutants, Chemical/toxicity*
  • Zebrafish/embryology
  • Zebrafish/growth & development
  • Zebrafish/physiology*
PubMed
24685621 Full text @ Aquat. Toxicol.
CTD
24685621
Abstract
The flame retardant tris(2-butoxyethyl) phosphate (TBEP) is a frequently detected contaminant in the environment, wildlife and human milk. The potentially toxic effects of TBEP and their underlying molecular mechanisms have not been elucidated. Here, zebrafish embryos were exposed to different concentrations of TBEP from 4hours of post-fertilization (hpf) to 120hpf, and effects on embryonic development and global protein expression patterns examined. Our results demonstrate that treatment with TBEP (0.8-100mg/L) causes a concentration- and time-dependent decrease in embryonic survival and the hatching percentage. The median lethal concentration was 10.7mg/L at 120hpf. Furthermore, exposure to 150 or 800 μg/L TBEP inhibited the degradation and utilization of vitellogenins and down-regulated the expression of proteins related to cation binding, and lipid transport, uptake and metabolism, accompanied by a decrease in heart rate and body length. Exposure to TBEP (150 or 800 μg/L) also decreased the expression of proteins involved in cell proliferation and DNA repair, and led to an increased number of apoptotic cells in the tail region. Collectively, our results suggest that exposure to TBEP causes toxicity in the developing zebrafish by inhibiting the degradation and utilization of nutrients from the mother and inducing apoptosis.
Genes / Markers
Figures
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping