Abstract

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 Ca 2+ 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 Ca 2+ 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 4 d prior to inhibition of net Ca 2+ 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 Ca 2+ 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 Ca 2+ 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.

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