Research article summary (published 21 Sep 2009):

Nanoparticles can induce changes in the intracellular metabolism of lipids without compromising cellular viability.

Full Abstract

There is growing concern about the safety of engineered nanoparticles, which are produced for various industrial applications. Quantum dots are colloidal semiconductor nanoparticles that have unique luminescence characteristics and the potential to become attractive tools for medical imaging. However, some of these particles can cause oxidative stress and induce cell death. The objective of this study was to explore quantum dot-induced metabolic changes, which could occur without any apparent cellular damage. We provide evidence that both uncoated and ZnS-coated quantum dots can induce the accumulation of lipids (increase in cytoplasmic lipid droplet formation) in two cell culture models: glial cells in primary mouse hypothalamic cultures and rat pheochromocytoma PC12 cells. Glial cells treated with CdTe quantum dots accumulated newly synthesized lipids in a phosphoinositide 3-kinase-dependent manner, which was consistent with the growth factor-dependent accumulation of lipids in PC12 cells treated with CdTe and CdSe/ZnS quantum dots. In PC12 cells, quantum dots, as well as the hypoxia mimetic CoCl(2), induced the up-regulation of hypoxia-inducible transcription factor-1alpha and the down-regulation of the beta-oxidation of fatty acids, both of which could contribute to the accumulation of lipids. On the basis of our results, we propose a model illustrating how nanoparticles, such as quantum dots, could trigger the formation of intracellular lipid droplets, and we suggest that metabolic measurements, such as the determination of fat oxidation in tissues, which are known sites of nanoparticle accumulation, could provide useful measures of nanoparticle safety. Such assays would expand the current platform of tests for the determination of the biocompatibility of nanomaterials.

Author information

Author/s: Przybytkowski, Ewa (E); Behrendt, Maik (M); Dubois, David (D); Maysinger, Dusica (D);

Affiliation: Department of Pharmacology and Therapeutics, McGill University, Montréal, Canada.

Journal and publication information

Publication Type: Journal Article; Research Support, Non-U.S. Gov't

Journal: The FEBS journal (FEBS J), published in England. (Language: eng)

Reference: 2009-Nov; vol 276 (issue 21) : pp 6204-17

Dates: Created 2009/10/14; Completed 2009/10/28;

PMID: 19780838, status: MEDLINE (last retrieved date: 10/28/2009)

Sourced from the National Library of Medicine. Abstract text and other information may be subject to copyright.

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MeSH headings (categories)

This article was linked to the MeSH Headings (categories) shown below.

1-Phosphatidylinositol 3-Kinase - physiology Animals Cell Survival Fatty Acids, Nonesterified - metabolism Lipid Metabolism Mice

Nanoparticles - toxicity Oxidation-Reduction PC12 Cells Quantum Dots Rats Signal Transduction

Note: Bold headings indicate primary MeSH headings or qualifiers.

Associated Chemicals: Fatty Acids, Nonesterified (0) ; 1-Phosphatidylinositol 3-Kinase (EC 2.7.1.137)

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