ZFIN ID: ZDB-PUB-190717-5
Functions of thioredoxin1 in brain development and in response to environmental chemicals in zebrafish embryos
Yang, L., Zeng, C., Zhang, Y., Wang, F., Takamiya, M., Strähle, U.
Date: 2019
Source: Toxicology letters   314: 43-52 (Journal)
Registered Authors: Strähle, Uwe, Takamiya, Masanari, Yang, Lixin
Keywords: Thioredoxin1, environmental toxicants, hydrocephalus, oxidative stress, zebrafish embryo
MeSH Terms:
  • Animals
  • Animals, Genetically Modified
  • Apoptosis/drug effects
  • Brain/drug effects*
  • Brain/embryology
  • Brain/metabolism
  • Embryo, Nonmammalian/drug effects
  • Embryo, Nonmammalian/metabolism
  • Embryo, Nonmammalian/pathology
  • Environmental Pollutants/toxicity*
  • Epithelial Cells/drug effects
  • Epithelial Cells/metabolism
  • Epithelial Cells/pathology
  • Gene Expression Regulation, Developmental
  • Hydrocephalus/chemically induced*
  • Hydrocephalus/embryology
  • Hydrocephalus/genetics
  • Hydrocephalus/metabolism
  • Neurons/drug effects
  • Neurons/metabolism
  • Neurons/pathology
  • Oxidative Stress/drug effects
  • Thioredoxins/genetics
  • Thioredoxins/metabolism*
  • Zebrafish/embryology
  • Zebrafish/genetics
  • Zebrafish/metabolism*
  • Zebrafish Proteins/genetics
  • Zebrafish Proteins/metabolism*
PubMed: 31310794 Full text @ Toxicol. Lett.
Thioredoxin is an evolutionarily conserved antioxidant protein that plays a crucial role for fundamental cellular processes and embryonic development. Growing evidence support that Thioredoxin influences cellular response to chemicals insults, particularly those accompanying oxidative stress. The mechanisms underlying the functions of Thioredoxin1 in the embryonic development under the environmental toxicant exposure remain, however, largely unexplored. We report here that thioredoxin1 becomes differentially expressed in zebrafish embryos after exposure to 9 out of 11 environmental chemicals. In situ gene expression analysis show that thioredoxin1 is expressed in neurons, olfactory epithelia, liver and swim bladder under normal conditions. After MeHg exposure, however, thioredoxin1 is ectopically induced in the hair cells of the lateral line and in epithelia cells of the pharynx. Knockdown of Thioredoxin1 induces hydrocephalus and increases cell apoptosis in the brain ventricular epithelia cells. In comparison with 5% malformation in embryos injected with control morpholino, MeHg induces more than 77% defects in Thioredoxin1 knockdown embryos. Our data suggest that there is an association between hydrocephalus and Thioredoxin1 malfunction in embryonic development, and provide valuable information to elucidate the protective role of Thioredoxin1 against chemicals disruption.