title: CdSe quantum dot (QD)-induced morphological and functional impairments to liver in mice.
abstract: Quantum dots (QDs), as unique nanoparticle probes, have been used in in vivo fluorescence imaging such as cancers. Due to the novel characteristics in fluorescence, QDs represent a family of promising substances to be used in experimental and clinical imaging. Thus far, the toxicity and harmful health effects from exposure (including environmental exposure) to QDs are not recognized, but are largely concerned by the public. To assess the biological effects of QDs, we established a mouse model of acute and chronic exposure to QDs. Results from the present study suggested that QD particles could readily spread into various organs, and liver was the major organ for QD accumulation in mice from both the acute and chronic exposure. QDs caused significant impairments to livers from mice with both acute and chronic QD exposure as reflected by morphological alternation to the hepatic lobules and increased oxidative stress. Moreover, QDs remarkably induced the production of intracellular reactive oxygen species (ROS) along with cytotoxicity, as characterized by a significant increase of the malondialdehyde (MDA) level within hepatocytes. However, the increase of the MDA level in response to QD treatment could be partially blunted by the pre-treatment of cells with beta-mercaptoethanol (β-ME). These data suggested ROS played a crucial role in causing oxidative stress-associated cellular damage from QD exposure; nevertheless other unidentified mediators might also be involved in QD-mediated cellular impairments. Importantly, we demonstrated that the hepatoxicity caused by QDs in vivo and in vitro was much greater than that induced by cadmium ions at a similar or even a higher dose. Taken together, the mechanism underlying QD-mediated biological influences might derive from the toxicity of QD particles themselves, and from free cadmium ions liberated from QDs as well.
authors: State Key Laboratory of Environmental Chemistry and Ecotoxicology, Research Center for Eco-Environmental Sciences, Chinese Academy of Sciences, Beijing, China.
authors: Wei
authors: W
authors: Liu
authors: Shuping
authors: S
authors: Zhang
authors: Lixin
authors: L
authors: Wang
authors: Chen
authors: C
authors: Qu
authors: Changwen
authors: C
authors: Zhang
authors: Lei
authors: L
authors: Hong
authors: Lin
authors: L
authors: Yuan
authors: Zehao
authors: Z
authors: Huang
authors: Zhe
authors: Z
authors: Wang
authors: Sijin
authors: S
authors: Liu
authors: Guibin
authors: G
authors: Jiang
mesh_terms: D000818:Animals; D019187:Cadmium Compounds / Q000737:chemistry / Q000633:toxicity*; D002460:Cell Line; D002469:Cell Separation; D005434:Flow Cytometry; D005979:Glutathione Peroxidase / Q000378:metabolism; D007477:Ions; D008099:Liver / Q000187:drug effects* / Q000378:metabolism*; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D008623:Mercaptoethanol / Q000494:pharmacology; D051379:Mice; D046529:Microscopy, Electron, Transmission / Q000379:methods; D015233:Models, Statistical; D018384:Oxidative Stress; D045663:Quantum Dots; D017382:Reactive Oxygen Species; D018036:Selenium Compounds / Q000737:chemistry / Q000633:toxicity*
chemical_list: D019187:Cadmium Compounds; D007477:Ions; D017382:Reactive Oxygen Species; D018036:Selenium Compounds; D008315:Malondialdehyde; D008623:Mercaptoethanol; C058667:cadmium selenide; D005979:Glutathione Peroxidase