Quantum dots enhance Cu2+-induced hepatic l02 cells toxicity: involvement of Nrf2

Both quantum dots- (QD) and copper- (Cu2+) induced reactive oxygen species (ROS) generation. The mechanisms underlying oxidative damage of combined QD and Cu were examined. Thus, the antioxidant enzyme glutathione-S-transferase (GST) enzyme activity and its genetic transcription regulator nuclear factor E2 (Nrf2) transcription factor expression was investigated in L02 cells. Addition of 2 mu g mL-1 (IC10) QD enhanced Cu2+-induced GST activity and Nrf2 transcription factor levels by 35% and 86%, respectively. QD and Cu increased toxicity was also confirmed by cell morphology changes. The findings that QD- and/or Cu2+-induced toxicity enhanced GST via the Nrf2/antioxidant response element (ARE) pathway indicate that oxidant stress resulted in antioxidant responses being initiated in hepatic cells possibly as an adaptive mechanism.