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Mutat Res. 2017 Oct;774:12-24. doi: 10.1016/j.mrrev.2017.08.003. Epub 2017 Aug 24.

Inflammation and the chemical carcinogen benzo[a]pyrene: Partners in crime.

Author information

1
Department of Pharmacology & Toxicology, NUTRIM School of Nutrition and Translational Research in Metabolism, Maastricht University, PO Box 616, 6200 MD, Maastricht, The Netherlands.
2
Department of Pharmacology & Toxicology, NUTRIM School of Nutrition and Translational Research in Metabolism, Maastricht University, PO Box 616, 6200 MD, Maastricht, The Netherlands; Departement of Pharmacology & Toxicology, NUTRIM School for Nutrition and Translational Research in Metabolism, Maastricht University, PO Box 616, 6200 MD, Maastricht, The Netherlands. Electronic address: F.vanschooten@maastrichtuniversity.nl.

Abstract

Exposure to benzo[a]pyrene (B[a]P) is known to play a role in lung carcinogenesis and the underlying processes can be modified by the presence of inflammation. The inflammatory process can for instance enhance the concentration of reactive metabolites that bind to DNA and may also diminish DNA repair. Additionally, during the inflammatory process mediators are released that create a microenvironment which is suitable for further stimulation of cancer development. Various transcriptional pathways are activated by inflammation, including pathways that are mediated via nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), signal transducer and activator of transcription 3 (STAT-3), and hypoxia-inducible factor-1 (HIF-1). Crosstalk between these pathways and the aryl hydrocarbon receptor (AhR) occurs at multiple levels and thereby boosts B[a]P induced carcinogenesis. This review focuses on inflammatory mediators, including cytokines, chemokines and extracellular enzymes that modulate molecular events in B[a]P induced cancers.

KEYWORDS:

Benzo[a]pyrene; Carcinogens; Cytochrom P450 1A1; Inflammation; Inflammatory mediators

PMID:
29173495
DOI:
10.1016/j.mrrev.2017.08.003
[Indexed for MEDLINE]

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