Molecular mechanism of copper-zinc superoxide dismutase activity change exposed to N-acetyl-L-cysteine-capped CdTe quantum dots-induced oxidative damage in mouse primary hepatocytes and nephrocytes.

Quantum dots (QDs) are engineered semiconductor nanocrystals with promising application in biomedicine, which have potential toxic effect on biomacromolecules by direct interaction and indirect impact in the body. In this work, the effect of N-acetyl-L-cysteine-capped CdTe quantum dots with fluorescence emission peak at 612 nm (QDs-612) on copper-zinc superoxide dismutase (Cu/ZnSOD) at molecular and cellular level was investigated using isothermal titration calorimetry, spectroscopic techniques, cell counting kit-8, and total SOD assay. The hydrophobic interaction between Cu/ZnSOD and QDs-612 caused static fluorescence quenching of the protein, which was spontaneous with binding constant calculated to be 3.28 × 10(5) L mol(-1). The microenvironment of tyrosine residues, skeleton, and secondary structure of Cu/ZnSOD were changed with adding QDs-612. The molecular Cu/ZnSOD activity was inhibited at different concentrations of QDs-612 as well as the intracellular Cu/ZnSOD activity after 2-h exposure. Compared with the cell viability of hepatocytes and nephrocytes (decreased markedly of the initial level) with higher concentrations of QDs-612 in the absence of vitamin C, the cell viability of these two primary cells increased in the presence of vitamin C, indicating the oxidative damage induced by QDs-612. Therefore, the inhibition of Cu/ZnSOD activity in these two primary cells may be caused by the oxidative damage of massive ROS or direct interaction with QDs-612. This work establishes a new approach to investigate the biological toxicity of CdTe QDs to biomacromolecule from both molecular and cellular perspectives and obtains experimental evidence to thoroughly study the toxicity of CdTe QDs in vivo.