PUBLICATION

Tri-n-butyl phosphate delays tissue repair by dysregulating neutrophil function in zebrafish

Authors
Wang, Y., Cheng, Z., Zhang, H., Li, S., Pan, Y., Zhang, W., Huang, S., He, X., Zou, F., Yuan, Z., Yan, W., Huang, H.
ID
ZDB-PUB-220612-1
Date
2022
Source
Toxicology and applied pharmacology   449: 116114 (Journal)
Registered Authors
Huang, Huizhe
Keywords
Chemotaxis, Neutrophil, Regeneration, Tri-n-butyl phosphate, Zebrafish
MeSH Terms
  • Animals
  • Larva
  • Neutrophils*
  • Organophosphates
  • Zebrafish*/genetics
  • Zebrafish Proteins/genetics
PubMed
35690110 Full text @ Tox. App. Pharmacol.
CTD
35690110
Abstract
Tri-n-butyl phosphate (TnBP) is a widely used organophosphate ester, but its effects on the regenerative process under damaging circumstances remain unknown. In the present study, zebrafish larvae were exposed to 0, 50, 100, 200 and 1000 μg/L TnBP, and the caudal fins were cut at 72 h post fertilization (hpf). First, after exposure to TnBP, the number of total neutrophils decreased together with decreased neutrophils in the tail, and TnBP inhibited chemotaxis. Second, reactive oxygen species (ROS) levels in the zebrafish decreased greatly. Following exposure to TnBP, transcription levels of many genes regulating fin regeneration, such as fgf20a, fgfr1a, bmp2a and bmp4, were significantly downregulated, while inflammatory factors such as cxcl8a, cxcl18b, il-6, and tnfa were abnormally upregulated. In addition, TnBP inhibited the regenerative area after caudal fin amputation. The inflammatory state was adverse during the regenerative process. In summary, TnBP exposure is immunotoxic and decreases oxidative stress in injured zebrafish larvae.
Genes / Markers
Figures
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping