Toxicity of cadmium quantum dots compared to cadmium and zinc ions in zebrafish (Danio rerio) and water flea (Daphnia pulex)



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Recent advances in the ability to manufacture and manipulate materials at the nanoscale have led to increased production and use of many types of nanomaterials in diverse areas. Nanocrystaline semiconductors (Quantum dots; QDs) are small, long-lived fluorescent nanocrystals composed of a core of semiconductor material (e.g. cadmium selenide, zinc sulfide) and shells or dopants of other elements. Often, the continuously increased uses of QDs come increased appearance of in the aqueous environments, and then can be toxic to aquatic organisms and poses significant ecological risks. However, the toxicological impacts of heavy metal constituted QDs on aquatic species are largely unknown, especially at the molecular level. Moreover, it is crucial to determine whether the toxicity of metallic QDs is quantitative or mechanistically different than that of soluble metal components. The aim of this study was to compare the toxicities of ionic cadmium (Cd) and zinc (Zn) and Cd- and Zn-containing QDs at both in vitro via zebrafish liver cells (ZFL) and in vivo through Daphnia pulex. Our results revealed that (1) ionic Cd2+ was more toxic than Zn2+, and the general trend of toxicity of QDs was determined to be CdTe > CdSe/ZnS or InP/ZnS; (2) smaller QDs showed greater toxicity than larger QDs; (3) both Cd2+ and CdTe QDs exposure led to an accumulation of Cd, an increased formation of intracellular reactive oxygen species (ROS), and an induction of DNA strand breaks; (4) CdTe QDs exposure induced expression patterns of metal response, stress defense, and DNA repair genes in a manner similar to that of Cd2+ exposure, while CdSe/ZnS or InP/ZnS QDs altered gene expression in a manner very different from that of the corresponding Cd or Zn salts; and (5) nucleotide excision repair (NER) repair capacity were inhibited with Cd2+ but not with CdTe. The adverse cellular effects caused by acute exposure of QDs might be mediated through differing mechanisms than those resulting from Cd2+ toxicity, and studying the effects of the ionic form may be not enough to explain QD toxicities in aquatic organisms.