Evidence map›Paper›PMID 24260113›Full record

ArticlePloS one2013

The extreme variety of genotoxic response to benzo[a]pyrene in three different human cell lines from three different organs.

Camille Genies, Anne Maître, Emmanuel Lefèbvre, Amandine Jullien, Marianne Chopard-Lallier, Thierry Douki

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
2.2field-weighted citation impact, top 13% 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

25 citing papers in PubMed, 71 citations in OpenAlex.

  1. Article
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  7. DNA adducts as link betweenCurrent research in toxicology · 2023
    Article
  8. Article
  9. Article
  10. Article
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  12. Article
  13. Modulatory Effects of Silymarin on Benzo[a]pyrene-Induced Hepatotoxicity.International journal of molecular sciences · 2020
    Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Modulation of benzo[a]pyrene-DNA adduct formation by CYP1 inducer and inhibitor.Genes and environment : the official journal of the Japanese Environmental Mutagen Society · 2017
    Review
  19. Article
  20. Petrol exposure and DNA integrity of peripheral lymphocytes.International archives of occupational and environmental health · 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

6 authors at 3 institutions in 1 country.

Camille GeniesLaboratoire « Lésions des Acides Nucléiques », Université Joseph Fourier - Grenoble 1/CEA/Institut Nanoscience et Cryogénie/SCIB, Grenoble, France ; Equipe EPSP Environnement et Prédiction de la Santé des Populations - laboratoire TIMC (UMR CNRS 5525), CHU de Grenoble, Université Joseph Fourier, UFR de médecine, Domaine de la Merci, La Tronche, France ; Agence de l'environnement et de la Maîtrise de l'Energie 20, Angers, France.
Anne Maître
Emmanuel Lefèbvre
Amandine Jullien
Marianne Chopard-Lallier
Thierry Douki
CEA Grenoble · FRUniversité Joseph Fourier · FRCentre Hospitalier Universitaire de Grenoble · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Polycyclic aromatic hydrocarbons (PAHs) are associated with occupational exposure and urban atmospheric pollution. Determination of the genotoxic properties of these compounds is thus of outmost importance. For this purpose a variety of cellular models have been widely used. Reliable results can however only be obtained with models reflecting the specific sensitivity of different organs towards PAHs. In this work, we compared the response to benzo[a]pyrene in cell lines from human lungs (A549) and bladder (T24); two important target organs for PAHs-induced cancer. Human hepatocytes (HepG2) were used as a reference, although liver is not a concern for PAHs carcinogenesis. Adducts arising from the ultimate diol-epoxide metabolite of B[a]P, BPDE, were found to be produced in a dose-dependent manner in HepG2. BPDE DNA adducts were not detected in T24 and in A549 their formation was found to be most efficient at the lowest concentration studied (0.2 µM). These results are probably explained by differences in induction and activity of phase I metabolization enzymes, as well as by proteins eliminating the B[a]P epoxide in A549. In addition to BPDE adducts, oxidative DNA damage, namely strand breaks and oxidized purines were measured and found to be produced only in minute amounts in all three cell lines. In summary, our results emphasize the large differences in the response of cells originating from different organs. Our data also point out the importance of carefully selecting the doses used in in vitro toxicological experiments. The example of A549 shows that working at high doses may lead to an underestimation of the risk. Finally, the choice of method for evaluating genotoxicity appears to be of crucial importance. The comet assay does not seem to be the best method for a compound like B[a]P which induces stable adducts causing limited oxidative damage.

Indexed as

DNA DamageAir Pollutants, OccupationalBenzo(a)pyreneDNA AdductsHep G2 CellsHumansOccupational ExposureOrgan SpecificityOxidation-ReductionAir Pollutants, OccupationalBenzo(a)pyreneDNA Adducts

Identifiers

PMID24260113
PMCPMC3832631
OpenAlexW1994634312

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.