TiO2 nanoparticles act as a carrier of Cd bioaccumulation in the ciliate Tetrahymena thermophila.

When nanoparticles can enter a unicellular organism directly, how may they affect the bioaccumulation and toxicity of other pollutants already present in the environment? To answer this question, we conducted experiments with a protozoan Tetrahymena thermophila. The well-dispersed polyacrylate-coated TiO2 nanoparticles (PAA-TiO2-NPs) were used as a representative nanomaterial, and Cd as a conventional pollutant. We found that PAA-TiO2-NPs could get into Tetrahymena cells directly. Such internalization was first induced by low concentrations of Cd, but later suppressed when Cd concentrations were higher than 1 µg/L. Considering its significant adsorption on PAA-TiO2-NPs, Cd could be taken up by T. thermophila in the form of free ion or metal-nanoparticle complexes. The latter route accounted for 46.3% of Cd internalization. During the 5 h depuration period, 4.34-22.1% of Cd was excreted out, which was independent of the concentrations of intracellular Cd and PAA-TiO2-NPs. On the other hand, both free and intracellular Cd concentrations only partly predicted its toxicity at different levels of PAA-TiO2-NPs. This may have resulted from PAA-TiO2-NPs' synergistic effects and the distinct subcellular distribution of Cd taken up via the two routes above. Overall, we should pay attention to the carrier effects of nanoparticles when assessing their environmental risks.

Cd2+ toxicity as affected by bare TiO2 nanoparticles and their bulk counterpart.

Toxicity of engineered nanoparticles has received extensive attention in recent years. However, nanoparticles always co-exist with other pollutants in natural environment. Whether there are any interactions between these classical pollutants and nanoparticles; and how these interactions may influence the environmental behavior, effects and fate of each other remain largely unclear. For this purpose, effects of bare titanium dioxide engineered nanoparticles (TiO(2)-NP) and their bulk counterpart (TiO(2)-BC) on Cd(2+) bioavailability and toxicity to the green alga Chlamydomonas reinhardtii were examined in the present study. We first investigated the kinetics and equilibrium isotherm of Cd(2+) adsorption on both particles in the algal culture medium. Pseudo-first-order adsorption kinetics was observed with equilibrium rate constant ranging from 0.19 to 0.33min(-1). Increase in Cd(2+) adsorption with its ambient concentration at equilibrium followed a single Langmuir isotherm for different concentrations of TiO(2). Furthermore, surface-area-based Cd(2+) adsorption by TiO(2)-BC was higher than that by TiO(2)-NP in most Cd(2+) concentration treatments suggesting that particle size was not the only cause for different adsorption. Both forms of TiO(2) could alleviate Cd(2+) inhibitive effects on C. reinhardtii. However, Cd(2+) toxicity and its bioaccumulation were comparable as long as its free ion concentration in ambient toxicity media was similar regardless the particle size and concentration of TiO(2). There was no TiO(2) inside the algal cells either. Therefore, it was Cd(2+) adsorption by TiO(2) which decreased its ambient free ion concentration and further its intracellular accumulation as well as toxicity.

Cd2+ Toxicity to a green alga Chlamydomonas reinhardtii as influenced by its adsorption on TiO2 engineered nanoparticles.

In the present study, Cd(2+) adsorption on polyacrylate-coated TiO(2) engineered nanoparticles (TiO(2)-ENs) and its effect on the bioavailability as well as toxicity of Cd(2+) to a green alga Chlamydomonas reinhardtii were investigated. TiO(2)-ENs could be well dispersed in the experimental medium and their pH(pzc) is approximately 2. There was a quick adsorption of Cd(2+) on TiO(2)-ENs and a steady state was reached within 30 min. A pseudo-first order kinetics was found for the time-related changes in the amount of Cd(2+) complexed with TiO(2)-ENs. At equilibrium, Cd(2+) adsorption followed the Langmuir isotherm with the maximum binding capacity 31.9, 177.1, and 242.2 mg/g when the TiO(2)-EN concentration was 1, 10, and 100 mg/l, respectively. On the other hand, Cd(2+) toxicity was alleviated in the presence of TiO(2)-ENs. Algal growth was less suppressed in treatments with comparable total Cd(2+) concentration but more TiO(2)-ENs. However, such toxicity difference disappeared and all the data points could be fitted to a single Logistic dose-response curve when cell growth inhibition was plotted against the free Cd(2+) concentration. No detectable amount of TiO(2)-ENs was found to be associated with the algal cells. Therefore, TiO(2)-ENs could reduce the free Cd(2+) concentration in the toxicity media, which further lowered its bioavailability and toxicity to C. reinhardtii.