Investigations into the mechanism of lead toxicity to the freshwater pulmonate snail, Lymnaea stagnalis.

The freshwater pulmonate snail, Lymnaea stagnalis, is the most sensitive aquatic organism tested to date for Pb with an estimated EC20 for juvenile snail growth of 3 μg l⁻¹. A previous study supported the hypothesis that this hypersensitivity to Pb was due to an extremely high Ca²⁺ uptake rate needed to support shell formation. The current study sought to build upon this working hypothesis and develop a mechanistic predictive model for inhibition of snail growth as a function of Pb exposure. Initial experiments confirmed previous predictions that juvenile snails have net Ca²⁺ uptake rates of 7000-8000 nmol g⁻¹ h⁻¹, approximately 100-fold higher than observed in a typical freshwater fish. However, an initial time course study revealed that the onset of growth inhibition occurs at least 4d prior to inhibition of net Ca²⁺ flux in Pb-exposed snails indicating the latter is not the primary mechanism of action. Qualitative observations during this experiment indicated snail feeding was inhibited in a dose-dependent manner. A subsequent experiment demonstrated that when food is withheld from snails for even 24 h, net Ca²⁺ uptake is significantly (∼50%) reduced. A second time course study demonstrated quantitatively that snail feeding is inhibited by Pb exposure by up to 98% at relatively high Pb concentrations (57 μg l⁻¹) but no inhibition was observed at ≤ 10 μg l⁻¹ Pb indicating feeding inhibition is not causing observed growth effects at concentrations approximating the EC20 of 3 μg l⁻¹ Pb. A final experiment testing whether Pb-induced growth effects are related to inhibition of carbonic anhydrase activity in the snail mantle also failed to demonstrate an effect. We conclude that while both feeding and net Ca²⁺ uptake in snails are affected by Pb exposure, they appear to be secondary effects. The primary mechanism of action explaining L. stagnalis hypersensitivity to Pb remains to be identified.