Brominated flame retardants (BFRs) represent a large group of chemicals used in a variety of household and commercial products to prevent fire propagation. The environmental persistence and toxicity of some of the most widely used BFRs has resulted in a progressive ban worldwide and the development of novel BFRs for which the knowledge on environmental health impacts remains limited. The objectives of this study were to evaluate the effects of two emerging BFRs, 1,2-bis(2,4,6-tribromophenoxy)ethane (BTBPE) and 2-ethylhexyl-2,3,4,5-tetrabromobenzoate (EH-TBB), in diet exposed juvenile rainbow trout (Oncorhynchus mykiss). Both compounds were detected in fish carcasses at 76% and 2% of the daily dosage of BTBPE and EH-TBB, respectively, indicating accumulation of BTBPE and by contrast extensive depuration/metabolism of EH-TBB. Liver gene transcription analysis using RNA-sequencing indicated that the chronic 28-d dietary exposure of trout to EH-TBB down-regulated one single gene related to endocrine-mediated processes, whereas BTBPE impacted the transcription of 33 genes, including genes involved in the immune response, reproduction, and oxidative stress. Additional analysis using qRT-PCR after 48-h and 28-d of exposure confirmed the impact of BTBPE on immune related genes in the liver (apolipoprotein A-I, lysozyme) and the head-kidney (complement c3-4). However, the activity of lysozymes measured at the protein level did not reflect transcriptomic results. Overall, results suggested an impact on immune-related gene transcription in BTBPE exposed fish, as well as oxidative stress and endocrine disruption potentials.

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Keywords BTBPE, EHTBB, Flame retardants, Gene transcription, Rainbow trout, RNA-sequencing
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Journal Aquatic Toxicology
Giraudo, M. (Maeva), Douville, M. (Mélanie), Letcher, R.J, & Houde, M. (Magali). (2017). Effects of food-borne exposure of juvenile rainbow trout (Oncorhynchus mykiss) to emerging brominated flame retardants 1,2-bis(2,4,6-tribromophenoxy)ethane and 2-ethylhexyl-2,3,4,5-tetrabromobenzoate. Aquatic Toxicology, 186, 40–49. doi:10.1016/j.aquatox.2017.02.023