Mercury-induced lipid category disruption and Na⁺/K⁺-ATPase inhibition in Cerastoderma edule gills

Mercury chloride (HgCl₂) represents a critical environmental pollutant due to its long-term persistence, high potential for bioaccumulation, and pronounced toxicity, which together contribute to serious disruptions in aquatic ecosystems. This study is the first to investigate changes in the lipid membrane composition, including subclasses and relative proportions, in the gills of Cerastoderma edule, and to explore how these alterations affect Na⁺/K⁺-ATPase activity following exposure to HgCl₂. C. edule individuals were exposed to sublethal concentrations of HgCl₂ (1, 10, and 100 μg/L) for 6 days, alongside a non-exposed control group. All treatment groups showed a significant rise in hydrogen peroxide levels compared to the control, which was accompanied by increased lipid peroxidation, as indicated by the elevated concentrations of lipid hydroperoxides. These oxidative changes may account for the disruption of gill membrane integrity, reflected by marked reductions in key phospholipids such as phosphatidylserine (PS), phosphatidylinositol (PI), phosphatidylcholine (PC), and phosphatidylethanolamine (PE). Significant alterations were also observed in associated lipid components, particularly polyunsaturated fatty acids (PUFAs), including n-3 and n-6 families, as well as key molecules such as docosahexaenoic acid (DHA), eicosapentaenoic acid (EPA), and arachidonic acid (ARA). These changes disrupted the membrane integrity and led to increased levels of neutral lipids, mainly triacylglycerol and cholesterol, accompanied by modifications in PUFA content, especially n-6 PUFA and their key constituents such as ARA and EPA, in HgCl₂-treated gills. Interestingly, these changes affected the activity of the Na⁺/K⁺-ATPase protein pump, causing depletion in all HgCl₂-treated specimens. This inhibition was associated with specific binding to phospholipids, which altered the rigidity of the cell's bilayer membrane, as evidenced in our study by variations in membrane fluidity and integrity ratios. These results highlight the specific toxicity of HgCl₂ regarding different phospholipids, cholesterol, and triglycerides, and their combined impact on the stability of Na⁺/K⁺-ATPase, thereby disrupting cellular homeostasis.