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 increased Cyp1a-1 transcription 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 the Cyp1a-1. These results suggest that the induction of Cyp1a-1 gene expression by myristicin in Hepa-1 cells might occur through an Ah receptor-independent pathway.
journal_name
Biochem Biophys Res Communjournal_title
Biochemical and biophysical research communicationsauthors
Jeong HG,Lee SS,Kim HK,Yang KHdoi
10.1006/bbrc.1997.6507subject
Has Abstractpub_date
1997-04-28 00:00:00pages
619-22issue
3eissn
0006-291Xissn
1090-2104pii
S0006-291X(97)96507-4journal_volume
233pub_type
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