Lipids, and their constitutive fatty acids, are key nutrients for fish health as they provide energy, maintain cell structure, are precursors of signalling molecules and act as nuclear receptor ligands. These specific roles may be of crucial importance in a context of exposure to pollutants. We recently showed that the fatty acid profile of rainbow trout liver cell phospholipids modulates sensitivity to an acute methylmercury challenge. In order to investigate mechanisms of effects, we herein tested whether specific polyunsaturated fatty acids (PUFAs) may protect cells from methylmercury through decreasing intracellular mercury accumulation and/or enhancing cellular defences (e.g. via modulation of gene expression patterns). We also investigated the inverse relationship and assessed the impact of methylmercury on cellular fatty acid metabolism. To do so, the fatty acid composition of rainbow trout liver cell phospholipids was first modified by incubating them in a medium enriched in a specific PUFA from either the n-3 family (alpha-linolenic acid, ALA; eicosapentaenoic acid, EPA) or the n-6 family (linoleic acid, LA; arachidonic acid, AA). Cells were then exposed to methylmercury (0.15 or 0.50 μM) for 24 h and sampled thereafter for assessing phospholipid fatty acid profile, intracellular total mercury burden, and expression pattern of genes involved in fatty acid metabolism, synthesis of PUFA-derived signalling molecules and stress response. We observed that cells incorporated the given PUFA and some biotransformation products in their phospholipids. Methylmercury had few impacts on this cellular phospholipid composition. None of the PUFA enrichments affected the cellular mercury burden, suggesting that the previously observed cytoprotection conferred by ALA and EPA was not linked to a global decrease in cellular accumulation of mercury. Fatty acid enrichments and methylmercury exposure both modulated gene expression patterns. Genes involved in the synthesis of PUFA-derived signalling molecules, in stress response and the orphan cytochrome P450 20A1 were identified as possible sites of interaction between fatty acids and methylmercury in rainbow trout liver cells.

脂质及其组成性脂肪酸是鱼类健康的关键营养物质，因为它们提供能量，维持细胞结构，是信号分子的前体并充当核受体配体。在暴露于污染物的情况下，这些特定的作用可能至关重要。我们最近显示，虹鳟鱼肝细胞磷脂的脂肪酸谱可调节对急性甲基汞挑战的敏感性。为了研究作用机理，我们在本文中测试了特定的多不饱和脂肪酸（PUFA）是否可以通过减少细胞内汞的积累和/或增强细胞防御能力（​​例如，通过调节基因表达模式）来保护细胞免受甲基汞的侵害。我们还研究了反比关系，并评估了甲基汞对细胞脂肪酸代谢的影响。为此，首先通过在富含n-3族（α-亚麻酸，ALA；二十碳五烯酸，EPA）的特定PUFA的培养基中孵育彩虹虹鳟肝细胞磷脂的脂肪酸组成，以对其进行修饰。 n-6族（亚油酸，洛杉矶；花生四烯酸，AA）。然后将细胞暴露于甲基汞（0.15或0.50μM）中24 h，然后取样以评估磷脂脂肪酸谱，细胞内总汞负荷以及与脂肪酸代谢有关的基因表达模式，PUFA衍生的信号分子的合成和应激回复。我们观察到细胞在其磷脂中掺入了给定的PUFA和一些生物转化产物。甲基汞对该细胞磷脂的组成影响很小。没有一种PUFA富集影响细胞汞的负担，这表明先前观察到的由ALA和EPA赋予的细胞保护作用与汞细胞蓄积的总体减少没有关系。脂肪酸富集和甲基汞暴露均调节基因表达模式。在应激反应和孤儿细胞色素P450 20A1中，涉及PUFA衍生信号分子合成的基因被确定为虹鳟肝细胞中脂肪酸与甲基汞之间相互作用的可能位点。