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. Author manuscript; available in PMC: 2021 Apr 21.
Published in final edited form as: J Occup Environ Med. 2019 Dec;61(Suppl 12):S82–S89. doi: 10.1097/JOM.0000000000001691

Figure 1: HpCDD and BghiP induce AHR-driven luciferase activity.

Figure 1:

(A) Chemical structures of polycyclic aromatic hydrocarbons (PAHs) and dibenzo-p-dioxins used in this study. The compounds are: 6-formylindolo[3,2-b]carbazole (FICZ), 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), 1,2,3,4,6,7,8-Heptachlorodibenzo-p-doxin (HpCDD), Benzo(ghi)perylene (BghiP) and Naphthalene. (B) HEK293FT cells were used to test if the chemicals affect AHR activity. The DRE-luciferase reporter construct (which harbors 2 dioxin response elements (DRE) upstream of the firefly luciferase gene) and the pCMV-AHR plasmid (which constitutively expresses human AHR) were introduced into cells as described in the online supplement. After 20 hours of exposure to the chemicals, cells were collected and luciferase activity measured. FICZ induced a robust increase in luciferase activity at both 100 nM and 1 µM. TCDD induced luciferase activity at 100 pM. HpCDD induced a dose-responsive increase in luciferase activity where 1–5 nM HpCDD elicited a similar response as 100 pM TCDD. BghiP induced a significant induction in DRE-luc at 2 µM. Naphthalene at 2 µM did not induce DRE-luciferase. The experiment was repeated two times in quadruplicate with a representative experiment shown and data presented as means + standard error., * = p < 0.05, ** = p < 0.01, *** = p < 0.001, One-way-ANOVA.