Inhibition of Gap Junction Intercellular Communications in Cell Culture by Polycyclic Aromatic Hydrocarbons (PAH) in the Absence of PAH Metabolism

Ju. Ju. Sharovskaja¹, A. V. Vaiman², N. A. Solomatina², and V. A. Kobliakov^2*

¹Belozersky Institute of Physico-Chemical Biology, Lomonosov Moscow State University, Moscow 119992, Russia

²Institute of Carcinogenesis, Blokhin Russian Cancer Research Center, Russian Academy of Medical Sciences, Moscow 115478, Russia; E-mail: vakob@crc.umos.ru

^* To whom correspondence should be addressed.

Received June 16, 2003; Revision received September 23, 2003

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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.

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KEY WORDS: gap junction intercellular communications, polycyclic aromatic hydrocarbons, Ah receptor

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