Journal
JOURNAL OF TOXICOLOGICAL SCIENCES
Volume 41, Issue 6, Pages 775-781Publisher
JAPANESE SOC TOXICOLOGICAL SCIENCES
DOI: 10.2131/jts.41.775
Keywords
Electrophile; Aryl hydrocarbon receptor; Quinone; CYP1A1
Categories
Funding
- Ministry of Education, Culture, Sports, Science, and Technology of Japan [JP25220103, JP15K18906]
- NIH [R01 ES006273, R01 ES010807]
- Grants-in-Aid for Scientific Research [15K18906] Funding Source: KAKEN
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While it has long been believed that benzenes and naphthalenes are unable to activate the aryl hydrocarbon receptor (AhR) because they are poor ligands, we recently reported that these quinoid metabolites upregulated cytochrome P450 1A1 (CYP1A1) in Hepalcic7 cells (Abiko et al., 2015). In the current study, AhR activation, measured with a bioluminescence-based cell free assay, was induced by 1,2-naphthoquinone (1,2-NQ), a metabolite of naphthalene. Consistent with this, 1,4-benzoquinone (1,4-BQ), tert-butyl-1,4-BQ, and 1,4-NQ, as well as 1,2-NQ, all electrophilic mono- and bi-cyclic quinones, upregulated CYP1A1 mRNA and protein in HepG2 cells, whereas their parent aromatic hydrocarbons had little effect. Furthermore, immunofluorescence analysis confirmed that these quinones enhanced translocation of AhR to the nucleus.
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