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Genotoxic capacity of Cd/Se semiconductor quantum dots with differing surface chemistries.

Manshian BB, Soenen SJ, Brown A, Hondow N, Wills J, Jenkins GJ, Doak SH - Mutagenesis (2015)

Bottom Line: However, our understanding of the toxicological structure-activity relationships remains limited.Carboxyl-QD demonstrated the smallest agglomerate size and greatest cellular uptake, which correlated with a dose dependent increase in cytotoxicity and genotoxicity.Oxidative stress and induced mitochondrial reactive oxygen species were only partially associated with cytotoxicity and genotoxicity induced by the QD, hence were not the only mechanisms of importance.

View Article: PubMed Central - PubMed

Affiliation: Institute of Life Science, College of Medicine, Swansea University, Singleton Park, Swansea SA2 8PP, UK, Biomedical NMR Unit-MoSAIC, Department of Medicine, KU Leuven, B-3000 Leuven, Belgium and.

No MeSH data available.


Related in: MedlinePlus

Point mutagenicity induced by QD. (A) Carboxyl-QD, (B) amine-QD, (C) HDA-QD exposed to TK6 cells for 18h. Results are presented as mean ± standard deviation (n = 3). Significance is indicated with *P ≤0.05 and **P ≤ 0.005.
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Figure 5: Point mutagenicity induced by QD. (A) Carboxyl-QD, (B) amine-QD, (C) HDA-QD exposed to TK6 cells for 18h. Results are presented as mean ± standard deviation (n = 3). Significance is indicated with *P ≤0.05 and **P ≤ 0.005.

Mentions: The mammalian hprt forward mutation assay was applied to quantify cells containing point mutations following QD exposure, where the positive control induced a MF of 197±70×10−6. Carboxyl-QD resulted in a dose-dependent increase of point mutations up to 10nM where an approximate 2-fold increase in MF was observed (Figure 5A) compared with the control levels. This increase in MF was however not maintained at the highest 15nM dose and those elevations in MF observed at the lower doses did not reach significance. Similarly, an increase in MF was observed in TK6 cells following exposure to 5 and 7.5nM concentrations of HDA-QD where approximately 3- and 2-fold increase in MF were recorded respectively, but this again did not reach significance (Figure 5C). In contrast, no noticeable mutagenicity was caused by exposure to the amine-QD (Figure 5B).


Genotoxic capacity of Cd/Se semiconductor quantum dots with differing surface chemistries.

Manshian BB, Soenen SJ, Brown A, Hondow N, Wills J, Jenkins GJ, Doak SH - Mutagenesis (2015)

Point mutagenicity induced by QD. (A) Carboxyl-QD, (B) amine-QD, (C) HDA-QD exposed to TK6 cells for 18h. Results are presented as mean ± standard deviation (n = 3). Significance is indicated with *P ≤0.05 and **P ≤ 0.005.
© Copyright Policy - creative-commons
Related In: Results  -  Collection

License 1 - License 2
Show All Figures
getmorefigures.php?uid=PMC4696518&req=5

Figure 5: Point mutagenicity induced by QD. (A) Carboxyl-QD, (B) amine-QD, (C) HDA-QD exposed to TK6 cells for 18h. Results are presented as mean ± standard deviation (n = 3). Significance is indicated with *P ≤0.05 and **P ≤ 0.005.
Mentions: The mammalian hprt forward mutation assay was applied to quantify cells containing point mutations following QD exposure, where the positive control induced a MF of 197±70×10−6. Carboxyl-QD resulted in a dose-dependent increase of point mutations up to 10nM where an approximate 2-fold increase in MF was observed (Figure 5A) compared with the control levels. This increase in MF was however not maintained at the highest 15nM dose and those elevations in MF observed at the lower doses did not reach significance. Similarly, an increase in MF was observed in TK6 cells following exposure to 5 and 7.5nM concentrations of HDA-QD where approximately 3- and 2-fold increase in MF were recorded respectively, but this again did not reach significance (Figure 5C). In contrast, no noticeable mutagenicity was caused by exposure to the amine-QD (Figure 5B).

Bottom Line: However, our understanding of the toxicological structure-activity relationships remains limited.Carboxyl-QD demonstrated the smallest agglomerate size and greatest cellular uptake, which correlated with a dose dependent increase in cytotoxicity and genotoxicity.Oxidative stress and induced mitochondrial reactive oxygen species were only partially associated with cytotoxicity and genotoxicity induced by the QD, hence were not the only mechanisms of importance.

View Article: PubMed Central - PubMed

Affiliation: Institute of Life Science, College of Medicine, Swansea University, Singleton Park, Swansea SA2 8PP, UK, Biomedical NMR Unit-MoSAIC, Department of Medicine, KU Leuven, B-3000 Leuven, Belgium and.

No MeSH data available.


Related in: MedlinePlus