Chronic tributyltin exposure induces metabolic disruption in an invertebrate model animal, Lymnaea stagnalis.

Over the last 20 years, tributyltin (TBT) has been reported to cause metabolic disruption in both invertebrates and vertebrates, highlighting the need for further detailed analysis of its physiological effects. This study aimed to investigate the metabolic-disrupting effects of TBT from the behavioral to the molecular level. Adult specimens of the great pond snail (Lymnaea stagnalis) were exposed to an environmentally relevant concentration (100 ng L-1) of TBT for 21 days. After the chronic exposure, behavioral alterations as well as histological, cellular, and molecular changes were investigated in the central nervous system, kidney, and hepatopancreas. TBT exposure significantly decreased feeding activity, while locomotor activity remained unchanged. At the histological level, the cellular localization of tin was demonstrated in all tissues investigated and, in addition, characteristic morphological changes were observed in the kidney and hepatopancreas. Tissue-specific changes in lipid profiles confirmed TBT-induced disruption of lipid homeostasis in mollusks, characterized by a consistent reduction in the proportion of polyunsaturated fatty acids and a shift toward more saturated lipids. The expression of 17β-hydroxysteroid dehydrogenase type 12 (HSD17B12) enzyme, involved in lipid metabolism in vertebrates, was reduced in all three tissues after TBT exposure. Our results show that TBT induces significant multi-level metabolic changes in Lymnaea, including direct alterations in feeding activity and lipid composition. Our findings also suggest that HSD17B12 enzyme plays a key role in lipid metabolism in mollusks, as in mammals, and is likely involved in TBT-induced metabolic disruption. Overall, our study extends the findings of previous studies on mollusks by providing novel behavioral as well as tissue-specific histological and metabolic data and highlights the complexity and evolutionary conserved way of TBT-induced metabolic disruption.