Abstract
We have studied the effect of polycyclic aromatic hydrocarbons (PAH) on gap junction intercellular communications (GJIC) in culture of hepatoma cells Hep G2 and G27. Carcinogenic PAH inhibited GJIC in both cultures in contrast to non-carcinogenic PAH. We showed that both constitutive and inducible expressions of mRNAs of Ah receptor and cytochrome P4501A1 (the main isoform involved in PAH metabolism) were absent in hepatoma G27 cells. We concluded that the initial, non-metabolized molecules of carcinogenic PAH are responsible for changes in GJIC through interaction with an unknown factor in the cellular membrane.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Base Sequence
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Benzo(a)pyrene / metabolism
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Benzo(a)pyrene / pharmacology
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Cell Communication / drug effects*
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Cell Line, Tumor
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Cells, Cultured
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Cytochrome P-450 CYP1A1 / genetics
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Cytochrome P-450 CYP1A1 / metabolism
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Gap Junctions / drug effects*
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Humans
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Molecular Sequence Data
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Polycyclic Aromatic Hydrocarbons / metabolism
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Polycyclic Aromatic Hydrocarbons / pharmacology*
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Quantitative Structure-Activity Relationship
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RNA, Messenger / metabolism
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Receptors, Aryl Hydrocarbon / genetics
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Receptors, Aryl Hydrocarbon / metabolism
Substances
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Polycyclic Aromatic Hydrocarbons
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RNA, Messenger
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Receptors, Aryl Hydrocarbon
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Benzo(a)pyrene
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Cytochrome P-450 CYP1A1