Application of the biotic ligand model to explain potassium interaction with thallium uptake and toxicity to plankton

Competitive interaction between TI(I) and K was successfully predicted by the biotic ligand model (BLM) for the microalga Chlorella sp. (Chlorophyta; University of Toronto Culture Collection strain 522) during 96-h toxicity tests. Because of a greater affinity of TI(I) (log K = 7.3-7.4) as compared to K (log K = 5.3-6.3) for biologically sensitive sites, an excess of 40- to 160-fold of K is required to suppress TI(I) toxic effects on Chlorella sp., regardless of [TI(I)] in solution. Similar excess of K is required to suppress TI(I) toxicity to Synechococcus leopoliensis (Cyanobacteria; University of Texas Culture Collection strain 625) and Brachionus calyciflorus (Rotifera; strain AB-RIF). The mechanism for the mitigating effect of K on TI(I) toxicity was investigated by measuring (TI)-T-204(I) cellular uptake flux and efflux in Chlorella sp. Potassium shows a competitive effect on TI(I) uptake fluxes that could be modeled using the BLM-derived stability constants and a Michaelis-Menten relationship. A strong TI efflux dependent only on the cellular TI concentration was measured. Although TI efflux does not explain the effect of K on TI(I) toxicity and uptake, it is responsible for a high turnover of the cellular TI pool (intracellular half-life = 12-13.5 min). No effect of Na+, Mg2+ or Ca2+ was observed on TI+ uptake, whereas the absence of trace metals (Cu, Co, Mo, Mn, Fe, and Zn) significantly increased TI uptake and decreased the mitigating effect of K+. The importance of K+ in determining the aquatic toxicity of TI+ underscores the use of ambient KI concentration in the establishment of TI water-quality guidelines and the need to consider K in predicting biogeochemical fates of TI in the aquatic environment.