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• W2396185588 abstract "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." @default.
• W2396185588 created "2016-06-24" @default.
• W2396185588 creator A5042967044 @default.
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• W2396185588 date "2016-05-23" @default.
• W2396185588 modified "2023-09-27" @default.
• W2396185588 title "Embryo Microinjection of Selenomethionine Reduces Hatchability and Modifies Oxidant Responsive Gene Expression in Zebrafish" @default.
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• W2396185588 doi "https://doi.org/10.1038/srep26520" @default.
• W2396185588 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4876371" @default.
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• W2396185588 hasPublicationYear "2016" @default.
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