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

Abstract

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 µg 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.

Keywords:

• QDs
• Nrf2
• GST
• L02 cell

Acknowledgments

We thank M.C. Chen for assistance with cell experiments and Z. Fang for providing QDs synthesis. Funding provided by the National Natural Science Foundation of China (no. 40871223), the Science and Technology Commission of Shanghai Municipality, China (no. 0752nm025).