Dietary vitamin A supplementation ameliorates the effects of poly-aromatic hydrocarbons in Atlantic salmon (Salmo salar)

•Plant-based salmon feeds requires vitamin A supplementation and increases PAH contamination.•Dietary vitamin A enhan ces PAH mediated CYP1A-biotransformation.•Dietary vitamin A and PAH interact on hepatic PAH accumulation, with reduced PAH in presence of vitamin A.•Dietary vitamin A restored PAH mediated reduced growth and reallocated energy storage and metabolism.

Several studies have reported on the interaction between vitamin A (VA) and aryl hydrocarbon receptor (AhR)-binding toxicants, including poly-aromatic hydrocarbons (PAHs). In aquaculture, the use of plant oils in novel aquafeeds can increase PAH levels while simultaneously lowering natural VA background levels, causing the need to supplement plant oil-based feeds with synthetic VA. To study dietary VA-PAH interactions, Atlantic salmon (initial weight 195 ± 0.15 g) were fed four identical plant-based diets that were supplemented with PAHs (100 and 10 mg kg−1 benzo[a]pyrene (BaP) and phenanthrene (Phe), respectively) or VA (retinyl acetate 8721 IU kg−1) separately or combined for 2.5 months in a 2 × 2 factorial design, with triplicate net-pens per diet. Dietary PAH significantly reduced hepatic VA storage, and VA-enriched diets restored hepatic VA. There was a significant PAH-VA interaction effect on hepatic BaP, but not Phe, accumulation, with reduced hepatic BaP concentrations in fish fed VA+PAH compared to fish fed PAH alone. Concurrently, PAH and VA significantly interacted in their effects on CYP1A phase I biotransformation as observed from increased ethoxyresorufin-O-deethylase (EROD) activity, increased CYP1A protein concentration, and elevated transcription (cyp1a1 gene expression) in fish fed PAH+VA compared to PAH alone. Dietary VA supplementation alone had no significant effect on CYP1A phase I biotransformation. Metabolomic assessment showed that dietary VA caused a restoration of metabolic intermediates involved in energy metabolism that were affected by dietary PAH. Moreover, a PAH-induced growth inhibition was partially ameliorated by dietary VA supplementation. In conclusion, dietary VA interacted with PAH toxicity on the level of CYP1A-mediated detoxification, hepatic PAH accumulation, energy allocation, and growth.