Application of the Biotic Ligand Model to Explain Potassium Interaction with Thallium Uptake and Toxicity to Plankton

摘要

Competitive interaction between T1(I) and K was successfully predicted by the biotic ligand model (BLM) for the microalga Chlorelia sp. (Chlorophyta; University of Toronto Culture Collection strain 522) during 96-h toxicity tests. Because ofrna 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-rnto l60-fold of K is required to suppress T1(I) toxic effects on Chlorelia sp., regardless of [T1(I)] in solution. Similar excess of Krns required to suppress T1(I) toxicity to Synechococcus leopoliensis (Cyanobacteria; University of Texas Culture Collection strain 625) and Brachionu: calyciflorus (Rotifera; strain AB-RIF). The mechanism for the mitigating effect of K on T1(I) toxicity wasrnnvestigated by measuring ~(204)Tl(I) cellular uptake flux and efflux in Chlorelia sp. Potassium shows a competitive effect on T1(I) uDtake fluxes that ceuld be modeled using the BLM-derived stability constants and a Michaelis-Menten relationship. A strong T1 efflux dependent only on the cellular T1 concentration was measured. Although T1 efflux does not explain the effect of K on T1(I) toxicity and uptake, it is responsible for a high turnover of the cellular T1 pool (intracellular half-life = 12-13.5 min). No effect of Na~+ Mg~(2+), or Ca~(2-) was observed on T1~+ uptake, whereas the absence of trace metals (Cu, Co, Mo, Mn, Fe, and Zn) significantly increased Tl uptake and decreased the mitigating effect of K~+. The importance of K~+ in determining the aquatic toxicity of T1~+ underscores the use of ambient K~+ concentration in the establishment of T1 water-quality guidelines and the need to consider K in predicting biogeochemical fates of T1 in the aquatic environment.