Contamination by tributyltin (TBT) has historically been one of the major threats to aquatic environments due to its rapid bioaccumulation and high toxicity even at low concentrations. Recent studies reported that TBT could alter lipid metabolism, pointing out that more detailed studies are required to understand its multifaceted impact in aquatic animals.Adult (4-5-month) specimens of the great pond snail (Lymnaea stagnalis) were exposed to 100 ng/L TBT for 21 days. Potential histological, cellular, and molecular alterations were investigated in the CNS, kidney, and hepatopancreas.In the CNS, tin was evenly distributed in all ganglia. Most tin compounds were located in the capsule and extracellular spaces. The neurons showed no remarkable morphological changes. Pathological alterations occurred in kidney and hepatopancreas. In these organs, the main targets of tin accumulation were epithelial. We identified hundreds of lipids in all tissues investigated. From the identified lipids, the amount of 17 lipids in the CNS and the amount of 31 lipids in both kidney and hepatopancreas changed significantly due to the chronic TBT exposure. We identified the homolog of HSD17B12 in Lymnaea and showed that its expression significantly decreased in all tissues due to the TBT treatment.Our findings showed that TBT could cause alterations at different biological levels and confirmed that it could induce changes in lipid metabolism in aquatic animals. Moreover, our results suggest that HSD17B12 enzyme in molluscs, as in mammals, is likely to be involved in lipid metabolism and had a highly conserved function during the animal evolution.