The potential toxic effects of nanoparticles are currently not well understood at the cellular level. Toxicity could result not only from the release of dissolved components, but from particle size and surface properties as well. This study assesses the in vitro reactivity of cadmium telluride quantum dots (CdTe QDs) in the presence of fish hepatocyte extracts and examines the (sub)lethal effects of CdTe QDs on rainbow trout hepatocytes. Cells were exposed to increasing concentrations of CdTe and dissolved cadmium for 48 h at 15^oC; cell viability, changes in intracellular Cd, lipid peroxidation, DNA strand break formation, molecular chaperone (Hsp72) and total ubiquitin levels were then examined. The incubation of CdTe to the post-mitochondrial fraction of hepatocytes led to significant loss of CdTe fluorescence with a concomitant decrease in labile Cd, indicating sequestration of Cd. The addition of Cd-binding proteins such as metallothioneins and glutathione significantly increased Cd mobility. Under oxidizing conditions, an increase in the loss of CdTe fluorescence with a decrease in Cd mobility was observed over time while, under reducing conditions (NADPH), a loss of fluorescence was prevented, with no observable change in Cd mobility. A physiological model for CdTe bioreactivity was proposed that shows that redox status and metal-binding proteins could modulate the fluorescence properties of the QDs. The exposure experiments revealed that both dissolved and colloidal Cd (i.e., CdTe QDs) were able to produce changes in the aforementioned effects, but the response pattern could not be solely attributed to dissolved Cd. The expression of the molecular chaperone Hsp72 and ubiquitin levels indicate that toxicity occurred through changes in protein conformation and tagging for elimination, which could be dependent also on nanoparticle size and geometry.

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