Evidence map›Paper›PMID 25441061›Full record

ArticleJournal of nanobiotechnology2014

Molecular mechanism of DNA damage induced by titanium dioxide nanoparticles in toll-like receptor 3 or 4 expressing human hepatocarcinoma cell lines.

Karim Samy El-Said, Ehab Mostafa Ali, Koki Kanehira, Akiyoshi Taniguchi

Open access · goldAbstract read
In one paragraph

Article in Journal of nanobiotechnology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
2.8field-weighted citation impact, top 9% of its field
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

20 citing papers in PubMed, 57 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Quercetin improves the apoptotic index and oxidative stress in post-thaw dog sperm.Environmental science and pollution research international · 2022
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  8. Review
  9. Article
  10. Article
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  13. Toxic Effects of TiO₂ NPs on Zebrafish.International journal of environmental research and public health · 2019
    Article
  14. Article
  15. Article
  16. Article
  17. Exposure to Engineered Nanomaterials: Impact on DNA Repair Pathways.International journal of molecular sciences · 2017
    Review
  18. Article
  19. Article
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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

4 authors at 4 institutions in 2 countries.

Karim Samy El-SaidCell-Material Interaction Group, Biomaterial Unit, Nano-Bio Field, Interaction Center for Material Nanoarchitectonics (MANA), National Institute for Materials Science (NIMS), Tsukuba, Japan. SAMYELSAIDALI.Karim@nims.go.jp.
Ehab Mostafa AliDepartment of Chemistry, Faculty of Science, Tanta University, Tanta, Egypt. ehab_1964@hotmail.com.
Koki KanehiraBiotechnology Group, TOTO Ltd. Research Institute, Honson 2-8-1, Chigasaki, Kanagawa, 253-8577, Japan. koki.kanehira@jp.toto.com.
Akiyoshi TaniguchiCell-Material Interaction Group, Biomaterial Unit, Nano-Bio Field, Interaction Center for Material Nanoarchitectonics (MANA), National Institute for Materials Science (NIMS), Tsukuba, Japan. taniguchi.akiyoshi@nims.go.jp.
National Institute for Materials Science · JPTanta University · EGToto (Japan) · JPWaseda University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundTitanium dioxide nanoparticles (TiO2 NPs) are widely used in the biological sciences. The increasing use of TiO2 NPs increases the risk of humans and the environment being exposed to NPs. We previously showed that toll-like receptors (TLRs) play an important role in the interactions between NPs and cells. Our previous results indicated that TLR4 increased the DNA damage response induced by TiO2 NPs, due to enhanced NP uptake into the cytoplasm, whereas TLR3 expression decreased the DNA damage response induced by TiO2 NPs because of NP retention in the endosome. In this study, we explored the molecular mechanism of the DNA damage response induced by TiO2 NPs using TLR3 or TLR4 transfected cells. We examined the effect of TLR3 or TLR4 over-expression on oxidative stress and the effect of DNA damage induced by TiO2 NPs on gene expression levels.

resultsOur results showed evidence for elevated oxidative stress, including the generation of reactive oxygen species (ROS), with increased hydrogen peroxide levels, decreased glutathione peroxidase, and reduced glutathione and activated caspase-3 levels in cells exposed for 48 h to 10 μg/ml TiO2 NPs. These effects were enhanced by TLR4 and reduced by TLR3 over-expression. Seventeen genes related to DNA double-strand breaks and apoptosis were induced, particularly IP6K3 and ATM.

conclusionOur results indicated that TiO2 NPs induced ROS, and the above molecules are implicated in the genotoxicity induced by TiO2 NPs.

Indexed as

DNA DamageGene Expression RegulationGlutathioneGlutathione PeroxidaseHep G2 CellsHumansHydrogen PeroxideNanoparticlesOxidative StressReactive Oxygen SpeciesReal-Time Polymerase Chain ReactionTitaniumToll-Like Receptor 3Toll-Like Receptor 4GlutathioneGlutathione PeroxidaseHydrogen PeroxideReactive Oxygen SpeciesTitaniumtitanium dioxideTLR3 protein, humanTLR4 protein, humanToll-Like Receptor 3Toll-Like Receptor 4

Identifiers

PMID25441061
PMCPMC4260178
OpenAlexW2109197874

What OpenQuestion holds

Textmetadata
LicenceCC BY
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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.