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.

Review of toxicological effect of quantum dots on the liver

“…IL‐1β is one of the most potent proinflammatory cytokines that can induce rapid recruitment of neutrophils to sites of inflammation, activate endothelial adhesion molecules, induce cytokines and chemokines, and stimulate specific types of adaptive immunity (Sahoo, Ceballos‐Olvera, del Barrio, & Re, ). This results were consistent with other research (Lin et al, ). The inflammation response in the liver from QDs was closely related to the Kupffer cells, which are responsible for removing exogenous substances in the liver.…”

“…However, there are some studies that have shown that QDs have no significant effect on liver function or pathological damage, but can cause mild inflammation on liver tissue (Haque et al, ; Lin et al, ; Liu et al, ; Lu et al, ; Stanca et al, ). Lin et al studied ICR mice injected intravenously with CdTe/ZnS (40 and 160 pmol per mouse).…”

“…Lin et al studied ICR mice injected intravenously with CdTe/ZnS (40 and 160 pmol per mouse). The results showed that the QDs did not cause any histopathological changes in the liver, but induced an elevated expression of some proinflammatory factors such as IL‐6 and TNF‐α, which suggested that it could create an immune response in the liver (Lin et al, ). IL‐6 is a cytokine that can induce differentiation of B cells, promote the growth and differentiation of primitive bone marrow‐derived cells with colony stimulating factor and enhance natural killer cell activity (Vallieres & Rivest, ).…”

Heme oxygenase expression as a biomarker of exposure to amphiphilic polymer-coated CdSe/ZnS quantum dots

“…Moreover, HMOX1 protein expression may be a very promising general biomarker for TOPO-PMAT QD exposure in vivo. Indeed, Lin and co-workers (Lin et al 2010) have recently shown that intravenous injection of CdTe QDs into mice caused an up-regulation of HMOX1, as well as other biomarkers of oxidative stress and inflammation, in the livers of these animals. While other organs were not evaluated, this report confirms that HMOX1 is a promising candidate biomarker of exposure to QDs in general.…”

Hepatotoxicity assessment of Mn-doped ZnS quantum dots after repeated administration in mice

“…18 Liu et al 7 found that CdSe QDs caused significant impairment to the liver by oxidative stress, as characterized by a significant increase in reactive oxygen species and malondialdehyde (MDA) levels within hepatocytes. Park et al 19 have suggested that bioconjugation could reduce the level of oxidative stress and decrease the toxicity of CdTe QDs to mammalian cells.…”