Abstract
Mouse hepatoma Hepa-1c1c7 (Hepa-1) cells were treated with myristicin to assess the role of myristicin in the process of Cyp1a-1 induction. Treatment of Hepa-1 cells with myristicin increasedCyp1a-1transcription in a dose-dependent manner as shown by analysis of 7-ethoxyresorufin O-deethylase activity, Cyp1a-1 protein level, and Cyp1a-1 mRNA. Myristicin, however, did not competitively displace [3H]2,3,7,8-tetrachlorodibenzo-p-dioxin from the Hepa-1 cytosolic aryl hydrocarbon (Ah) receptor in a competitive Ah receptor binding analysis using sucrose density gradient sedimentation and did not affect formation of DNA-protein complexes between the Ah receptor and its DRE target in a gel mobility shift assay using oligonucleotides corresponding to DRE 3 of theCyp1a-1.These results suggest that the induction ofCyp1a-1gene expression by myristicin in Hepa-1 cells might occur through an Ah receptor-independent pathway.
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