Impact of a primary wastewater effluent on liver lipid metabolism and oxidative stress in St. Lawrence River Northern pike

Municipal wastewater effluents (MWWEs) contain complex chemical mixtures that can affect the health of exposed aquatic organisms. Montreal's (Quebec, Canada) primary MWWE is one of the largest in North America and is a known point of release of halogenated flame retardants (HFRs) and per- and polyfluoroalkyl substances (PFAS) into the St. Lawrence River ecosystem. The objective of this study was to investigate hepatic lipid metabolism and oxidative stress in St. Lawrence River Northern pike (Esox lucius) environmentally exposed to Montreal's MWWE. A suite of HFRs and PFAS were also measured in pike liver. Among the 76 PFAS that were investigated in pike, 18 compounds were analyzed for the first time in St. Lawrence River fish, although only three of these could be detected and quantified. Concentrations of ∑₇₆PFAS in liver of female pike collected downstream of the effluent outfall were 32 % lower than those collected upstream. In male pike liver, 0.3-fold lower mRNA levels of peroxisome proliferator-activated receptor alpha (pparα), a regulator of lipid metabolism, and 0.7-fold lower levels of phospholipase A2 mRNA (pla2g4ab), involved in lysophosphatidylcholine and arachidonic acid metabolism, were observed. Additionally, there was a 17 % decrease in relative abundance of the ∑₁₅₂₈lipid at the downstream site for males. Higher percentages of contribution to the ∑₁₅₂₈lipid were noted for ∑₁₁₀₃membrane lipids (26 % higher) and ∑₂steroid lipids (50 % higher) in male pike collected at the downstream site. Moreover, negative correlations between ∑₃₄PBDE concentrations and pparα mRNA levels as well as between ∑₂steroid lipids and pla2g4ab mRNA levels were determined in male pike. These findings suggest that chronic environmental exposure of a top predator fish to a primary MWWE may have sex-specific effects on liver lipid content and composition as well as the transcription of genes involved in lipid metabolism.