The aryl hydrocarbon receptor-mediated and genotoxic effects of fractionated extract of standard reference diesel exhaust particle material in pulmonary, liver and prostate cells

2015 ◽  
Vol 29 (3) ◽  
pp. 438-448 ◽  
Author(s):  
Lenka Pálková ◽  
Jan Vondráček ◽  
Lenka Trilecová ◽  
Miroslav Ciganek ◽  
Kateřina Pěnčíková ◽  
...  
Keyword(s):  
Aryl Hydrocarbon Receptor ◽  
Diesel Exhaust ◽  
Diesel Exhaust Particle ◽  
Genotoxic Effects ◽  
Aryl Hydrocarbon ◽  
Prostate Cells ◽  
Particle Material

scholarly journals Diesel Exhaust Particle Toxicity on Spermatogenesis in the Mouse is Aryl Hydrocarbon Receptor Dependent

2007 ◽  
Vol 53 (5) ◽  
pp. 1069-1078 ◽  
Author(s):  
Hiromi IZAWA ◽  
Machiko KOHARA ◽  
Gen WATANABE ◽  
Kazuyoshi TAYA ◽  
Masaru SAGAI
Keyword(s):  
Aryl Hydrocarbon Receptor ◽  
Diesel Exhaust ◽  
Diesel Exhaust Particle ◽  
Aryl Hydrocarbon

scholarly journals E-cigarette Aerosol Condensate Enhances Metabolism of Benzo(a)pyrene to Genotoxic Products, and Induces CYP1A1 and CYP1B1, Likely by Activation of the Aryl Hydrocarbon Receptor

2019 ◽  
Vol 16 (14) ◽  
pp. 2468 ◽  
Author(s):  
Yuan-Wan Sun ◽  
Wieslawa Kosinska ◽  
Joseph B. Guttenplan
Keyword(s):  
Aryl Hydrocarbon Receptor ◽  
Cell Line ◽  
Tobacco Smoke ◽  
Genotoxic Effects ◽  
Aryl Hydrocarbon ◽  
Hydrolysis Products ◽  
Spontaneous Hydrolysis ◽  
Tobacco Carcinogen ◽  
Keratinocyte Cell ◽  
Carcinogenic Metabolite

E-cigarette aerosol contains lower levels of most known carcinogens than tobacco smoke, but many users of e-cigarettes are also smokers, and these individuals may be vulnerable to possible promoting and/or cocarcinogenic effects of e-cigarettes. We investigated the possibility that a condensate of e-cigarette aerosol (EAC) enhances the metabolism of the tobacco carcinogen, benzo(a)pyrene (BaP), to genotoxic products in a human oral keratinocyte cell line. Cells were pretreated with EAC from two popular e-cigs and then with BaP. Metabolism to its ultimate carcinogenic metabolite, anti-7,8-dihydroxy-9,10-epoxy-7,8,9,10-tetrahydro B[a]P (BPDE), was assayed by measuring isomers of its spontaneous hydrolysis products, BaP tetrols. The pretreatment of cells with EAC enhanced the rate of BaP tetrol formation several fold. Pretreatment with the e-liquid resulted in a smaller enhancement. The treatment of cells with EAC induced CYP1A1/1B1 mRNA and protein. The enhancement of BaP tetrol formation was inhibited by the aryl hydrocarbon receptor (AhR) inhibitor, α-napthoflavone, indicating EAC likely induces CYP1A1/1B1 and enhances BaP metabolism by activating the AhR. To our knowledge, this is first report demonstrating that e-cigarettes can potentiate the genotoxic effects of a tobacco smoke carcinogen.

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