Evidence map›Paper›PMID 26275419›Full record

ArticleMutagenesis2016

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

Bella B Manshian, Stefaan J Soenen, Andy Brown, Nicole Hondow, John Wills, Gareth J S Jenkins, Shareen H Doak

Abstract read
In one paragraph

Article in Mutagenesis, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

7 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. AnTurkish journal of pharmaceutical sciences · 2019
    Article
  7. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors.

Bella B ManshianInstitute 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.
Stefaan J SoenenBiomedical NMR Unit-MoSAIC, Department of Medicine, KU Leuven, B-3000 Leuven, Belgium and.
Andy BrownInstitute for Materials Research, SCaPE, University of Leeds, Leeds LS2 9JT, UK.
Nicole HondowInstitute for Materials Research, SCaPE, University of Leeds, Leeds LS2 9JT, UK.
John WillsInstitute of Life Science, College of Medicine, Swansea University, Singleton Park, Swansea SA2 8PP, UK.
Gareth J S JenkinsInstitute of Life Science, College of Medicine, Swansea University, Singleton Park, Swansea SA2 8PP, UK.
Shareen H DoakInstitute of Life Science, College of Medicine, Swansea University, Singleton Park, Swansea SA2 8PP, UK, s.h.doak@swansea.ac.uk.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Quantum dots (QD) have unique electronic and optical properties promoting biotechnological advances. However, our understanding of the toxicological structure-activity relationships remains limited. This study aimed to determine the biological impact of varying nanomaterial surface chemistry by assessing the interaction of QD with either a negative (carboxyl), neutral (hexadecylamine; HDA) or positive (amine) polymer coating with human lymphoblastoid TK6 cells. Following QD physico-chemical characterisation, cellular uptake was quantified by optical and electron microscopy. Cytotoxicity was evaluated and genotoxicity was characterised using the micronucleus assay (gross chromosomal damage) and the HPRT forward mutation assay (point mutagenicity). Cellular damage mechanisms were also explored, focusing on oxidative stress and mitochondrial damage. Cell uptake, cytotoxicity and genotoxicity were found to be dependent on QD surface chemistry. Carboxyl-QD demonstrated the smallest agglomerate size and greatest cellular uptake, which correlated with a dose dependent increase in cytotoxicity and genotoxicity. Amine-QD induced minimal cellular damage, while HDA-QD promoted substantial induction of cell death and genotoxicity. However, HDA-QD were not internalised by the cells and the damage they caused was most likely due to free cadmium release caused by QD dissolution. 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. Colloidal stability, nanoparticle (NP) surface chemistry, cellular uptake levels and the intrinsic characteristics of the NPs are therefore critical parameters impacting genotoxicity induced by QD.

Indexed as

DNA DamageOxidative StressSemiconductorsCadmiumCell LineHumansLymphocytesMutagenicity TestsMutagensQuantum DotsSeleniumStructure-Activity RelationshipSurface PropertiesCadmiumMutagensSelenium

Identifiers

PMID26275419
PMCPMC4696518

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.