The biological activity of quantum dots (QDs) is discussed very controversially and ranges from reports describing no adverse effects to studies showing immense toxicity [1-6]. These discrepancies depend on multiple factors including physico-chemical properties of the QDs themselves as well as environmental/experimental conditions [4].

 

Quantum dots (QDs) can be produced from a variety of different materials and they often have different coatings, thus, it cannot be expected that they provoke the same biological response in different cell lines or animals. In vitro toxicity studies have been performed in a variety of different cell types with an even bigger set of different or differently modified QDs. As a general rule physico-chemical properties such as size, core and shell material, stability of the shell material, type of coating, the production process as well as the surface charge of QDs can influence their biological effects. Furthermore, the cell type(s) in which toxicological measurements are being performed as well as the analysed concentration range have a major effect on the obtained results [3,4,6].

 

The QD core can be protected from degradation and release of e.g. toxic Cd2+ ions by various coatings [2,3,7,8]. The stability of the QD thus largely depends on the stability of its shell and/or coating material. How stable QDs are inside living cells or even organisms (see section “exposure - in vivo") strongly depends on their intracellular localisation (see section ”behaviour of uptake in somatic cells” ) [9].

In contrast to the protective effect of such coatings the material used to shield the core could itself affect cellular viability [2]. The coating material should thus be chosen very carefully. Furthermore excessive coating will increase the size or the hydrodynamic diameter (HD) of the QDs. This parameter becomes very important in animals during the process of excretion (see section “behaviour inside the body”).

 

Besides the release of Cd2+ ions the cytotoxicity of QDs has also been explained by the induction of reactive oxygen species (ROS) [8-10]. In high amounts these free radicals can induce damage to intracellular proteins, lipids and nucleic acids which can subsequently lead to cell death [9]. The subcellular distribution of Cadmium-Telluride (CdTe) -QDs has been shown to be size-dependent in two different cell types. While smaller QDs (2 nm) localise to the nuclear compartment larger ones (5 nm) localise to the cytosol [13]. Furthermore the same study reports that cytotoxicity is more pronounced with positively-charged smaller QDs compared to equally-charged larger QDs.

In addition Guo and colleagues report that positively-charged QDs lead to significant cell death in liver cells [7] indicating that surface charge of QDs has some effect on cell viability. In contrast to some of the results described above, another group of scientists shows – using again two other cell types – that the size of QDs does not influence their uptake and distribution. Moreover, no toxic effects of the QDs can be observed for up to ten days [14].

 

So far it is not clear if the QD has to enter a cell in order to exhibit negative effects or if an exterior contact between the QD and the cell is sufficient. The cytotoxicity of QDs has been described to correlate much better with intracellular concentrations of QDs than with extracellular exposure levels [15]. Furthermore the researchers conclude that this toxicity is mainly due to degradation of the particles and with that the release of toxic Cd2+ ions. This observation correlates very well with results discussed above. On the contrary other scientists could also show that the mere precipitation of QDs on the cell surface is enough to impair cell viability, though in a different manner compared to ingested particles [3].

In addition to cytotoxicity in general, damaging effects towards the genetic material (DNA) of a cell was assessed in several studies [8,10,16]. DNA strand breaks could be observed with and without exposure to light maybe involving reactive oxygen species [10,16]. Moreover the core or core-shell material respectively seems to determine the severity of DNA damage. While Cadmium-Telluride (CdTe) core particles showed the highest DNA damaging activity, CdTe/SiO2 core-shell particles were less potent and Manganese:Zinc-Selenide (Mn:ZnSe) particles induced almost no DNA damage [8].

 

 

Literature arrow down

  1. Derfus, AM et al. (2004), Nano Letters, 4(1): 11-18.
  2. Hoshino, A et al. (2004), Nano Letters, 4(11): 2163-2169.
  3. Kirchner, C et al. (2005), Nano Letters, 5(2): 331-338.
  4. Hardman, R (2006), Environ Health Perspect, 114(2): 165-172.
  5. Cho, SJ et al. (2007), Langmuir, 23(4): 1974-1980.
  6. Bottrill, M et al. (2011), Chem Commun (Camb), 47(25): 7039-7050.
  7. Guo, GN et al. (2007), Materials Letters, 61(8-9): 1641-1644.
  8. Wang, C et al. (2010), Talanta, 80(3): 1228-1233.
  9. Maysinger, D et al. (2007), Eur J Pharm Biopharm, 65(3): 270-281.
  10. Green, M et al. (2005), Chem Commun (Camb),(1): 121-123.
  11. Lu, HY et al. (2006), J Med Biol Eng, 26(2): 89-96.
  12. Chen, N et al. (2012), Biomaterials, 33(5): 1238-1244.
  13. Lovric, J et al. (2005), J Mol Med (Berl), 83(5): 377-385.
  14. Parak, WJ et al. (2002), Advanced Materials, 14(12): 882-885.
  15. Chang, E et al. (2006), Small, 2(12): 1412-1417.
  16. Anas, A et al. (2008), J Phys Chem B, 112(32): 10005-10011.

 

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