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Chem Res Toxicol. 2019 Aug 19;32(8):1491-1503. doi: 10.1021/acs.chemrestox.8b00397. Epub 2019 Jul 11.

Biodistribution and Systemic Effects in Mice Following Intravenous Administration of Cadmium Telluride Quantum Dot Nanoparticles.

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Environmental Health Science and Research Bureau, Healthy Environments and Consumer Safety Branch , Health Canada , 50 Colombine Driveway , Ottawa , Ontario , Canada K1A 0K9.
Department of Biology and Institute of Biochemistry , Carleton University , 1125 Colonel By Drive , Ottawa , Ontario Canada , K1S 5B6.
Bureau of Chemical Safety , Health Products and Food Branch , 251 Sir Frederick Banting Driveway , Health Canada, Ottawa , Ontario , Canada K1A 0K9.
University of Ottawa , Department of Biology, Centre for Advanced Research in Environmental Genomics and the Collaborative Program in Chemical and Environmental Toxicology , 75 Laurier Avenue East , Ottawa , Ontario , Canada K1N 6N5.


Quantum dots (QDs) are engineered nanoparticles (NPs) of semiconductor structure that possess unique optical and electronic properties and are widely used in biomedical applications; however, their risks are not entirely understood. This study investigated the tissue distribution and toxic effects of cadmium telluride quantum dots (CdTe-QDs) in male BALB/c mice for up to 1 week after single-dose intravenous injections. CdTe-QDs were detected in the blood, lung, heart, liver, spleen, kidney, testis and brain. Most CdTe-QDs accumulated in the liver, followed by the spleen and kidney. At high doses, exposure to CdTe-QDs resulted in mild dehydration, lethargy, ruffled fur, hunched posture, and body weight loss. Histological analysis of the tissues, upon highest dose exposures, revealed hepatic hemorrhage and necrotic areas in the spleen. The sera of mice treated with high doses of CdTe-QDs showed significant increases in alanine aminotransferase (ALT), aspartate aminotransferase (AST), and total bilirubin levels, as well as a reduction in albumin. CdTe-QD exposure also led to a reduced number of platelets and elevated total white blood cell counts, including monocytes and neutrophils, serum amyloid A, and several pro-inflammatory cytokines. These results demonstrated that the liver is the main target of CdTe-QDs and that exposure to CdTe-QDs leads to hepatic and splenic injury, as well as systemic effects, in mice. By contrast, cadmium chloride (CdCl2), at an equivalent concentration of cadmium, appeared to have a different pharmacokinetic pattern from that of CdTe-QDs, having minimal effects on the aforementioned parameters, suggesting that cadmium alone cannot fully explain the toxicity of CdTe-QDs.

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