Cd/Se/Te-based quantum dot 705 modulated redox homeostasis with hepatotoxicity in mice

Abstract

The objective of this study was to investigate whether quantum dot 705 (QD705) disrupts the cellular antioxidant systems leading to hepatotoxicity in mice. Mice were intravenously injected with QD705 and then sacrificed at week 12 or 16. Homeostasis of antioxidant-related metals, antioxidant activities, induction of oxidative stress, and toxicity in the liver were investigated. Although no histopathological change was observed, a time- and dose-dependent increase in metallothionein expression and reduction in liver function was noticed. Increased copper, zinc, and selenium levels and enhancements of the trace metal-corresponding transporters were noted at week 12. At week 16, a decline of selenium from its elevated level at week 12 was observed, which was accompanied by changes in glutathione peroxidase activity as well as in redox status. A significant reduction in superoxide dismutase activity was observed at 16 weeks. Furthermore, a corresponding elevation of heme oxygenase-1 expression, 8-oxo-7,8-dihydro-2′-deoxyguanosine, interleukin-6 and tumor necrosis factor-alpha suggested the presence of oxidative stress, oxidative DNA damage and inflammation.

Keywords::

• Nanoparticles
• QD705
• cadmium
• mice
• oxidative DNA damage
• hepatotoxicity

Declaration of interest: This work was supported by grant NM-097-PP08 and NM-098-PP08 from the Center for Nanomedicine Research, National Health Research Institutes, Zhunan, Taiwan. The authors report no conflict of interest. The authors alone are responsible for the content and writing of the paper.