Molecular mechanism of CAT and SOD activity change under MPA-CdTe quantum dots induced oxidative stress in the mouse primary hepatocytes.

Quantum dots (QDs) are a unique class of nano-materials that have attractive potentials in biological and biomedical applications, and the concern on their biosafety is concomitantly increasing. The overproduction of reactive oxygen species (ROS) is considered to be one of the reasons that induce the in vitro QDs induced toxic response. However, the exact molecular pathways underlying these effects remain poorly clarified and few studies combine the molecular results with the cellular results to explore the cytotoxic effect of QDs. The aim of the present study was to evaluate the effect of mercaptopropionic acid (MPA) capped CdTe QDs on the structures and functions of two antioxidant enzymes, catalase (CAT) superoxide dismutase (SOD), and then associated with the cytotoxic effects of oxidative stress induced by MPA-CdTe QDs on mouse hepatocytes to define the toxic underlying mechanism. The molecular experiment results showed that the exposure of QDs significantly changed the conformation of CAT and SOD, and leading to the promotion of molecular CAT activity and the inhibition of molecular SOD activity. Meanwhile, the cellular experiment results demonstrated that exposure to QDs changed the activities of CAT and SOD in mouse primary hepatocytes, led to the break of redox balance and resulted in the oxidative stress and cell apoptosis. This study explores the effects of MPA- CdTe QDs to the CAT and SOD molecules and then demonstrates the subsequent QDs toxic effects at a cellular level, revealing their potential risk in biomedical applications.