PUBLICATION

Embryo Microinjection of Selenomethionine Reduces Hatchability and Modifies Oxidant Responsive Gene Expression in Zebrafish

Authors
Thomas, J.K., Janz, D.M.
ID
ZDB-PUB-160524-7
Date
2016
Source
Scientific Reports   6: 26520 (Journal)
Registered Authors
Janz, David M.
Keywords
Animal physiology, Environmental impact, Metabolic syndrome
MeSH Terms
  • Animals
  • Embryo, Nonmammalian/drug effects*
  • GA-Binding Protein Transcription Factor/genetics
  • Gene Expression Regulation, Developmental/drug effects
  • Selenomethionine/administration & dosage
  • Selenomethionine/toxicity*
  • Zebrafish Proteins/genetics*
  • Zebrafish/embryology*
  • Zebrafish/genetics
  • Oxidative Stress
  • Receptors, Aryl Hydrocarbon/genetics
  • Teratogenesis
  • Selenium Radioisotopes/administration & dosage
  • Selenium Radioisotopes/toxicity*
  • Microinjections
(all 15)
PubMed
27210033 Full text @ Sci. Rep.
Abstract
In previous studies we demonstrated that exposure to selenomethionine (SeMet) causes developmental toxicities in zebrafish (Danio rerio). The objectives of this study were to establish a dose-response relationship for developmental toxicities in zebrafish after embryo microinjection of Se (8, 16 or 32 μg/g dry mass of eggs) in the form of SeMet, and to investigate potential underlying mechanism(s) of SeMet-induced developmental toxicities. A dose-dependent increase in frequencies of mortality and total deformities, and reduced hatchability were observed in zebrafish exposed to excess Se via embryo microinjection. The egg Se concentration causing 20% mortality was then used to investigate transcript abundance of proteins involved in antioxidant protection and methylation. Excess Se exposure modified gene expression of oxidant-responsive transcription factors (nuclear factor erythroid 2-related factor nrf2a and nrf2b), and enzymes involved in cellular methylation (methionine adenosyltransferase mat1a and mat2ab) in zebrafish larvae. Notably, excess Se exposure up-regulated transcript abundance of aryl hydrocarbon receptor 2 (ahr2), a signalling pathway involved in the toxicity of dioxin-related compounds. Our findings suggest that oxidative stress or modification of methylation, or a combination of these mechanisms, might be responsible for Se-induced developmental toxicities in fishes.
Genes / Markers
Figures
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Expression
Phenotype
No data available
Mutations / Transgenics
No data available
Human Disease / Model
No data available
Sequence Targeting Reagents
No data available
Fish
No data available
Antibodies
No data available
Orthology
No data available
Engineered Foreign Genes
No data available
Mapping
No data available
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Citation
Thomas, J.K., Janz, D.M. (2016) Embryo Microinjection of Selenomethionine Reduces Hatchability and Modifies Oxidant Responsive Gene Expression in Zebrafish. Scientific Reports. 6:26520.