A value of p < 0 05 was considered as statistically significant

A value of p < 0.05 was considered as statistically significant. Spectral and size properties of CdTe-QDs that were used in this study have been recently published by us (Nguyen et al., 2013). Cytotoxicity of CdTe-QDs in HepG2 cells was examined for changes in bioreducing activity using the MTT assay to estimate cellular capacity to reduce

MTT to its formazan. Loss in HepG2 bioreduction caused by CdTe-QDs appeared to be time- and dose-dependent (Fig. 1). The earliest changes were observed at 6 h with 1.0 μg/ml, and the lowest observable effects were observed with 0.1 μg/ml at 12 h exposure. At the longest exposure duration (24 h), CdTe-QDs caused a significant drop R428 in bioreduction at all doses, with maximal effects being ∼25% relative to control. Examination by microscopy showed that, even at this high

dose and exposure, cells had not detached (data not shown) and most still PR-171 order retained at least some capacity to reduce MTT to formazan, albeit at a much lower level compared to PBS-treated controls. The effect of CdTe-QDs on the production of ROS was examined by observing fluorescence of oxidized DHE in HepG2 by confocal microscopy. CdTe-QD treatment caused increased intensity and area of fluorescence from DHE oxidation compared to PBS-controls, indicating that excess ROS levels were induced by CdTe-QDs (Fig. 2A, B and E). Both CdCl2 and menadione treatments also showed an increase in ROS levels in test cells. CdCl2 treatment, however, caused a lower level of ROS generation than CdTe-QD treatment (p < 0.05) ( Fig. 2A–E). Several oxidative stress markers were selected to measure the effects of CdTe-QDs on the oxidative status of HepG2 cells. Exposures of HepG2 cells to CdTe-QDs caused a significant

depletion of reduced glutathione (GSH) (Fig. 3A). Furthermore, CdTe-QDs caused drops in the GSH/GSSG ratio by 2.4-fold, compared to PBS treated controls (Fig. 3A and B). CdCl2 caused a greater depletion of reduced GSH (p < 0.05), but a lower effect on the GSH/GSSG ratio compared to CdTe-QDs (p < 0.05) ( Fig. 3A and B). SOD activity was measured in both cytosolic and mitochondrial fractions (Fig. 3C). About 30% increase in SOD activity, in both cytosolic and mitochondrial extracts, occurred with CdTe-QD treatment. CdCl2 treatment also resulted in increased cytosolic and mitochondrial SOD activities, but to a lesser extent, Paclitaxel mouse compared to CdTe-QD treatment. Nrf2 activation was found to be 2-fold (p < 0.001) greater in CdTe-QD-treated cells, compared with control cells ( Fig. 3D), whereas CdCl2 caused a marginal increase (1.11-fold) in Nrf2 activation ( Fig. 3D). Compared to PBS-treated control cells, CdTe-QDs caused a reduction in GST activity by 1.95-fold (p < 0.001) and CdCl2 also caused a significant decrease in GST activity (1.65-fold, p < 0.001). To determine whether the decrease in GST activity was due to CdTe-QDs reducing GST protein levels directly, quantification of GST-α was performed.

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