Evidence map›Paper›PMID 25911668›Full record

ArticleToxicological sciences : an official journal of the Society of Toxicology2015

Pulmonary Inflammation Impacts on CYP1A1-Mediated Respiratory Tract DNA Damage Induced by the Carcinogenic Air Pollutant Benzo[a]pyrene.

Volker M Arlt, Annette M Krais, Roger W Godschalk, Yanira Riffo-Vasquez, Iveta Mrizova, Candice A Roufosse, Charmaine Corbin, Quan Shi, Eva Frei, Marie Stiborova and 3 more

Open access · bronzeAbstract read
In one paragraph

Article in Toxicological sciences : an official journal of the Society of Toxicology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
4.3field-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

37 citing papers in PubMed, 79 citations in OpenAlex.

  1. Article
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  3. Review
  4. Article
  5. Article
  6. Metabolic Activation of Benzo[International journal of molecular sciences · 2022
    Article
  7. Article
  8. Article
  9. Article
  10. Benzo[International journal of molecular sciences · 2021
    Article
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  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Targeted High Resolution LC/MSFrontiers in chemistry · 2019
    Article
  18. Article
  19. Article
  20. 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

13 authors at 5 institutions in 4 countries.

Volker M Arlt*Analytical and Environmental Sciences Division, MRC-PHE Centre for Environment & Health, King's College London, London SE1 9NH, United Kingdom, volker.arlt@kcl.ac.uk.
Annette M Krais*Analytical and Environmental Sciences Division, MRC-PHE Centre for Environment & Health, King's College London, London SE1 9NH, United Kingdom.
Roger W GodschalkDepartment of Toxicology, School for Nutrition, Toxicology and Metabolism (NUTRIM), Maastricht University Medical Centre, 6200 MD Maastricht, The Netherlands.
Yanira Riffo-VasquezSackler Institute of Pulmonary Pharmacology, Institute of Pharmaceutical Science, King's College London, London SE1 9NH, United Kingdom.
Iveta MrizovaDepartment of Biochemistry, Faculty of Science, Charles University, 12840 Prague 2, Czech Republic;
Candice A RoufosseDepartment of Histopathology, Imperial College Healthcare NHS Trust, Hammersmith Hospital, London W12 0HS, United Kingdom, and.
Charmaine Corbin*Analytical and Environmental Sciences Division, MRC-PHE Centre for Environment & Health, King's College London, London SE1 9NH, United Kingdom.
Quan ShiDepartment of Toxicology, School for Nutrition, Toxicology and Metabolism (NUTRIM), Maastricht University Medical Centre, 6200 MD Maastricht, The Netherlands.
Eva FreiDivision of Preventive Oncology, National Center for Tumor Diseases, German Cancer Research Center (DKFZ), Im Neuenheimer Feld 280, 69120 Heidelberg, Germany.
Marie StiborovaDepartment of Biochemistry, Faculty of Science, Charles University, 12840 Prague 2, Czech Republic;
Frederik-Jan van SchootenDepartment of Toxicology, School for Nutrition, Toxicology and Metabolism (NUTRIM), Maastricht University Medical Centre, 6200 MD Maastricht, The Netherlands.
David H Phillips*Analytical and Environmental Sciences Division, MRC-PHE Centre for Environment & Health, King's College London, London SE1 9NH, United Kingdom.
Domenico SpinaSackler Institute of Pulmonary Pharmacology, Institute of Pharmaceutical Science, King's College London, London SE1 9NH, United Kingdom.
King's College London · GBCharles University · CZMaastricht University Medical Centre · NLMaastricht University · NLNational Center for Tumor Diseases · DE

Funding

Cancer Research UK 14329Cancer Research UK C313/A14329Wellcome Trust 101 126/B/13/ZWellcome Trust 101 126/Z/12/Z
6 · The paper itself

Abstract

Pulmonary inflammation can contribute to the development of lung cancer in humans. We investigated whether pulmonary inflammation alters the genotoxicity of polycyclic aromatic hydrocarbons (PAHs) in the lungs of mice and what mechanisms are involved. To model nonallergic acute inflammation, mice were exposed intranasally to lipopolysaccharide (LPS; 20 µg/mouse) and then instilled intratracheally with benzo[a]pyrene (BaP; 0.5 mg/mouse). BaP-DNA adduct levels, measured by (32)P-postlabeling analysis, were approximately 3-fold higher in the lungs of LPS/BaP-treated mice than in mice treated with BaP alone. Pulmonary Cyp1a1 enzyme activity was decreased in LPS/BaP-treated mice relative to BaP-treated mice suggesting that pulmonary inflammation impacted on BaP-induced Cyp1a1 activity in the lung. Our results showed that Cyp1a1 appears to be important for BaP detoxification in vivo and that the decrease of pulmonary Cyp1a1 activity in LPS/BaP-treated mice results in a decrease of pulmonary BaP detoxification, thereby enhancing BaP genotoxicity (ie, DNA adduct formation) in the lung. Because less BaP was detoxified by Cyp1a1 in the lungs of LPS/BaP-treated mice, more BaP circulated via the blood to extrapulmonary tissues relative to mice treated with BaP only. Indeed, we observed higher BaP-DNA adduct levels in livers of LPS/BaP-treated mice compared with BaP-treated mice. Our results indicate that pulmonary inflammation could be a critical determinant in the induction of genotoxicity in the lung by PAHs like BaP. Cyp1a1 appears to be involved in both BaP bioactivation and detoxification although the contribution of other enzymes to BaP-DNA adduct formation in lung and liver under inflammatory conditions remains to be explored.

Indexed as

DNA DamageAir PollutantsAnimalsBenzo(a)pyreneCarcinogensCytochrome P-450 CYP1A1MaleMiceMice, Inbred C57BLPneumoniaRespiratory SystemAir PollutantsBenzo(a)pyreneCarcinogensCYP1A1 protein, humanCytochrome P-450 CYP1A1benzo[a]pyrenebronchoalveolar lavagecarcinogen metabolismcytochrome P450DNA adductspulmonary inflammation

Identifiers

PMID25911668
PMCPMC4517052
OpenAlexW2147457081

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.