Evidence map›Paper›PMID 20398356›Full record

ArticleParticle and fibre toxicology2010

Carbon black and titanium dioxide nanoparticles elicit distinct apoptotic pathways in bronchial epithelial cells.

Salik Hussain, Leen C J Thomassen, Ioana Ferecatu, Marie-Caroline Borot, Karine Andreau, Johan A Martens, Jocelyne Fleury, Armelle Baeza-Squiban, Francelyne Marano, Sonja Boland

Open access · goldAbstract read
In one paragraph

Article in Particle and fibre toxicology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
72citing papers in PubMed, 1 pooled it
10.3field-weighted citation impact, top 1% 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

72 citing papers in PubMed, 1 synthesis or guideline pooled it, 236 citations in OpenAlex.

  1. Pooled it
  2. Hepatotoxicity of titanium dioxide nanoparticles.Journal of applied toxicology : JAT · 2025
    Review
  3. Review
  4. Review
  5. Magneto-Mechanical Actuation Induces Endothelial Permeability.ACS biomaterials science & engineering · 2023
    Article
  6. Article
  7. Aerosol physicochemical determinants of carbon black and ozone inhalation co-exposure induced pulmonary toxicity.Toxicological sciences : an official journal of the Society of Toxicology · 2023
    Article
  8. Review
  9. Review
  10. Review
  11. Article
  12. Article
  13. Article
  14. Could Iron-Nitrogen Doping Modulate the Cytotoxicity of TiONanomaterials (Basel, Switzerland) · 2022
    Article
  15. Article
  16. Cytotoxicity of Particulate Matter PMJournal of toxicology · 2022
    Article
  17. Article
  18. Article
  19. Article
  20. Article

12 more citing papers are in PubMed but not listed here.

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

10 authors at 4 institutions in 3 countries.

Salik HussainUniversité Paris Diderot - Paris 7, Unit of Functional and Adaptive Biology (BFA) CNRS EAC 4413, Laboratory of Molecular and Cellular Responses to Xenobiotics, 75205 Paris, France.
Leen C J Thomassen
Ioana Ferecatu
Marie-Caroline Borot
Karine Andreau
Johan A Martens
Jocelyne Fleury
Armelle Baeza-Squiban
Francelyne Marano
Sonja Boland
Centre National de la Recherche Scientifique · FRUniversité Paris Cité · FRKU Leuven · BEInserm · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundIncreasing environmental and occupational exposures to nanoparticles (NPs) warrant deeper insight into the toxicological mechanisms induced by these materials. The present study was designed to characterize the cell death induced by carbon black (CB) and titanium dioxide (TiO2) NPs in bronchial epithelial cells (16HBE14o- cell line and primary cells) and to investigate the implicated molecular pathways.

resultsDetailed time course studies revealed that both CB (13 nm) and TiO2(15 nm) NP exposed cells exhibit typical morphological (decreased cell size, membrane blebbing, peripheral chromatin condensation, apoptotic body formation) and biochemical (caspase activation and DNA fragmentation) features of apoptotic cell death. A decrease in mitochondrial membrane potential, activation of Bax and release of cytochrome c from mitochondria were only observed in case of CB NPs whereas lipid peroxidation, lysosomal membrane destabilization and cathepsin B release were observed during the apoptotic process induced by TiO2 NPs. Furthermore, ROS production was observed after exposure to CB and TiO2 but hydrogen peroxide (H2O2) production was only involved in apoptosis induction by CB NPs.

conclusionsBoth CB and TiO2 NPs induce apoptotic cell death in bronchial epithelial cells. CB NPs induce apoptosis by a ROS dependent mitochondrial pathway whereas TiO2 NPs induce cell death through lysosomal membrane destabilization and lipid peroxidation. Although the final outcome is similar (apoptosis), the molecular pathways activated by NPs differ depending upon the chemical nature of the NPs.

Indexed as

Apoptosisbcl-2-Associated X ProteinBronchiCaspasesCell LineCell MembraneCell SizeCell SurvivalChromatinCytochromes cDNA FragmentationHumansHydrogen PeroxideLipid PeroxidationLysosomesMembrane Potential, MitochondrialBAX protein, humanbcl-2-Associated X ProteinCaspasesChromatinCytochromes cHydrogen PeroxideReactive Oxygen SpeciesSootTitaniumtitanium dioxide

Identifiers

PMID20398356
PMCPMC2873464
OpenAlexW2141864709

What OpenQuestion holds

Textmetadata
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.