Evidence map›Paper›PMID 22419868›Full record

ArticleInternational journal of nanomedicine2012

Titanium dioxide induces apoptotic cell death through reactive oxygen species-mediated Fas upregulation and Bax activation.

Ki-Chun Yoo, Chang-Hwan Yoon, Dongwook Kwon, Kyung-Hwan Hyun, Soo Jung Woo, Rae-Kwon Kim, Eun-Jung Lim, Yongjoon Suh, Min-Jung Kim, Tae Hyun Yoon and 1 more

Open access · goldAbstract read
In one paragraph

Article in International journal of nanomedicine, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
4.2field-weighted citation impact, top 5% 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

30 citing papers in PubMed, 69 citations in OpenAlex.

  1. Assessment of ion release, cytotoxicity, and potential systemic toxicity of titanium dental alloy.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2026
    Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Could Iron-Nitrogen Doping Modulate the Cytotoxicity of TiONanomaterials (Basel, Switzerland) · 2022
    Article
  7. Evaluating the Use of TiOInternational journal of nanomedicine · 2022
    Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. TiOFood science and biotechnology · 2019
    Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Photodynamic N-TiOScientific reports · 2016
    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

11 authors at 2 institutions in 2 countries.

Ki-Chun YooLaboratory of Molecular Biochemistry, Department of Chemistry, Hanyang University, Seoul, Republic of Korea.
Chang-Hwan Yoon
Dongwook Kwon
Kyung-Hwan Hyun
Soo Jung Woo
Rae-Kwon Kim
Eun-Jung Lim
Yongjoon Suh
Min-Jung Kim
Tae Hyun Yoon
Su-Jae Lee
Hanyang University · KRLymphoma Research Foundation · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundTitanium dioxide (TiO(2)) has been widely used in many areas, including biomedicine, cosmetics, and environmental engineering. Recently, it has become evident that some TiO(2) particles have a considerable cytotoxic effect in normal human cells. However, the molecular basis for the cytotoxicity of TiO(2) has yet to be defined. METHODS AND

resultsIn this study, we demonstrated that combined treatment with TiO(2) nanoparticles sized less than 100 nm and ultraviolet A irradiation induces apoptotic cell death through reactive oxygen species-dependent upregulation of Fas and conformational activation of Bax in normal human cells. Treatment with P25 TiO(2) nanoparticles with a hydrodynamic size distribution centered around 70 nm (TiO(2) (P25-70)) together with ultraviolet A irradiation-induced caspase-dependent apoptotic cell death, accompanied by transcriptional upregulation of the death receptor, Fas, and conformational activation of Bax. In line with these results, knockdown of either Fas or Bax with specific siRNA significantly inhibited TiO(2)-induced apoptotic cell death. Moreover, inhibition of reactive oxygen species with an antioxidant, N-acetyl-L-cysteine, clearly suppressed upregulation of Fas, conformational activation of Bax, and subsequent apoptotic cell death in response to combination treatment using TiO(2) (P25-70) and ultraviolet A irradiation.

conclusionThese results indicate that sub-100 nm sized TiO(2) treatment under ultraviolet A irradiation induces apoptotic cell death through reactive oxygen species-mediated upregulation of the death receptor, Fas, and activation of the preapoptotic protein, Bax. Elucidating the molecular mechanisms by which nanosized particles induce activation of cell death signaling pathways would be critical for the development of prevention strategies to minimize the cytotoxicity of nanomaterials.

Indexed as

Apoptosisbcl-2-Associated X ProteinCaspasesCell Linefas ReceptorHumansMembrane Potential, MitochondrialParticle SizeReactive Oxygen SpeciesRNA, Small InterferingTitaniumUp-Regulationbcl-2-Associated X ProteinCaspasesfas ReceptorReactive Oxygen SpeciesRNA, Small InterferingTitaniumtitanium dioxideapoptotic cell deathBax activationcaspase activationFas upregulationmitochondrial membrane potential lossreactive oxygen speciesTiO2

Identifiers

PMID22419868
PMCPMC3298386
OpenAlexW1857468255

What OpenQuestion holds

Textmetadata
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.