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.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Allylbenzene Derivatives
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Animals
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Benzyl Compounds*
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Cytochrome P-450 CYP1A1 / biosynthesis*
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Cytochrome P-450 CYP1A1 / genetics
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Dioxolanes / metabolism
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Dioxolanes / pharmacology*
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Enzyme Induction / drug effects
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Gene Expression / drug effects
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Liver Neoplasms, Experimental / enzymology*
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Liver Neoplasms, Experimental / genetics
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Liver Neoplasms, Experimental / metabolism
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Mice
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Polychlorinated Dibenzodioxins / metabolism
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Polychlorinated Dibenzodioxins / pharmacology
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Pyrogallol / analogs & derivatives
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RNA, Messenger / genetics
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RNA, Messenger / metabolism
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RNA, Neoplasm / genetics
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RNA, Neoplasm / metabolism
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Receptors, Aryl Hydrocarbon / metabolism
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Tumor Cells, Cultured
Substances
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Allylbenzene Derivatives
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Benzyl Compounds
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Dioxolanes
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Polychlorinated Dibenzodioxins
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RNA, Messenger
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RNA, Neoplasm
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Receptors, Aryl Hydrocarbon
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Pyrogallol
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myristicin
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Cytochrome P-450 CYP1A1