Mechanistic examination of thallium and potassium interactions in Daphnia magna

The trace element thallium (Tl) exerts its toxic effects, at least in part, through its mimicry of potassium (K⁺) and subsequent impairment of K⁺ homeostasis. However, the specific nature of this effect remains poorly understood, especially in aquatic biota that are threatened by elevated concentrations of Tl associated with mining and refining effluents. In this study experiments were conducted to mechanistically examine the relationship between Tl and K⁺ in terms of uptake and toxicity in the regulatory model species Daphnia magna. In one set of experiments the effects of K⁺, the K⁺ analog rubidium (Rb⁺), and generalized K⁺ channel blocker cesium (Cs⁺) on Tl-induced acute toxicity were examined. The presence of increasing concentrations of K⁺ and Rb⁺ in exposure water reduced waterborne Tl toxicity, indicating that the actions of Tl were mediated at least in part through interactions with K⁺. However, in the presence of elevated water Cs⁺, the toxicity of Tl paradoxically increased. Pharmaceuticals with putative blocking actions on K⁺ channels failed to alter whole-body K⁺ of control organisms, but in the case of clozapine and chlorpropamide, whole-body K⁺ status was significantly elevated relative to exposures with Tl alone, which tended to reduce this metric. These data identify inwardly rectifying and voltage gated K⁺ channels as potential loci of Tl toxicity. Experiments using rubidium (Rb⁺) as a tracer of K⁺, showed that waterborne Tl affects the uptake of K⁺, but the magnitude of inhibition by Tl was not sufficient to explain the effect on whole-body K⁺. While these data indicate interactions between Tl and K occur at K⁺ transporters in D magna, they also indicate that environmental levels of K⁺ are likely to ameliorate toxicity in most natural waters.