7-fold, p < 0 001) in mitochondrial Bax, but resulted in a modera

7-fold, p < 0.001) in mitochondrial Bax, but resulted in a moderate change in cytosolic Bax (1.2-fold, p < 0.05), compared to the control ( Fig. 8B). CdCl2 and STS exhibited similar effects as CdTe-QDs ( Fig. 8B). Since cytochrome c is released from mitochondria into cytosol in response to pro-apoptotic stimuli, its effect during CdTe-QDs exposure was examined. For

this, the levels of both cytosolic and mitochondrial cytochrome c during CdTe-QD exposure were compared. Results showed that CdTe-QDs caused reduced mitochondrial cytochrome c level (1.26-fold, p < 0.001), but an increase in cytosolic level (1.26-fold, p < 0.001), Dasatinib purchase compared to the control ( Fig. 8C). CdCl2 and STS exposures also showed similar effects ( Fig. 8C). MAPKs such as JNK, p38 and Erk1/2 have been shown to play important roles in apoptotic regulation by way of enzymatic activation through phosphorylation of tyrosine and threonine within their catalytic domains (Wada and Penninger, 2004). Using probes to quantify phosphorylation levels of these MAPKs showed that treatment of CdTe-QDs caused significant increases in levels of phosphorylated JNK, p38 and Erk(1/2) levels (12.8-, 9.0- and 7.5-fold (p < 0.001), respectively), compared to the control ( Fig. 8D). Similar treatments with CdCl2 and STS also resulted in significant increases (p < 0.001) in phosphorylation

of these MAPKs, compared to the control, but at lower levels, check details compared to CdTe-QDs (p < 0.05) ( Fig. 8D). In a recent study using well-characterized CdTe-QDs we demonstrated cytotoxic effects on murine macrophage J774A.1 and human epithelial HT29 cells (Nguyen et al., 2013). Here we extend this work by using HepG2 cells to model potential mechanisms of hepatocyte toxicity Sinomenine relating

to their exposure to CdTe-QDs. Initial work showed that CdTe-QD effects occurred in a dose- and time-dependent manner, consistent with our previous findings using the same source of CdTe-QDs. While the CdTeQDs used here are not identical to those used in other studies, the study results are largely consistent with past work using different cell lines and HepG2 (Su et al., 2009, Zhang et al., 2007 and Lovric et al., 2005). Su et al. (2009) showed that treatments of 0.1875–3 μM CdTe-QDs to human K562 erythroleukemia and human HEK293T embryonic kidney cells for 30 min to 48 h caused changes in bioreduction of MTT in a dose- and time-dependent manner. Similarly, Zhang et al. (2007) reported that treatments of 0–100 μM CdTe-QDs for 48 h to HepG2 cells induced cytotoxicity in a dose-dependent manner and proposed that Cd2+ ions were responsible for the cytototoxicity of the NPs. Lovric et al. (2005) also showed that CdTe-QDs caused cytotoxicity in the human breast cancer cell line MCF-7 in a dose-dependent manner after treatment of 1, 5, and 10 μg/ml CdTe-QDs for 24 h, but the authors claimed that QDs caused cytotoxicity exclusively by inducing ROS formation.

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