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
- Microinjections
- Oxidative Stress
- Receptors, Aryl Hydrocarbon/genetics
- Selenium Radioisotopes/administration & dosage
- Selenium Radioisotopes/toxicity*
- Selenomethionine/administration & dosage
- Selenomethionine/toxicity*
- Teratogenesis
- Zebrafish/embryology*
- Zebrafish/genetics
- Zebrafish Proteins/genetics*
- PubMed
- 27210033 Full text @ Sci. Rep.
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.
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
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping