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© 1996 Oxford University Press

other

The Effects of Anthracene and Methylated Anthracenes on Gap Junctional Intercellular Communication in Rat Liver Epithelial Cells

B. L. UPHAM*,{dagger},1, L. M. WEIS{dagger}, A. M. RUMMEL{ddagger}, S. J. MASTEN{dagger} and J. E. TROSKO*

*Department of Pediatrics and Human Development, Michigan State University East Lansing, Michigan 48824 {dagger}Department of Civil and Environmental Engineering, Michigan State University East Lansing, Michigan 48824 {ddagger}National Food Safety and Toxicology Center, Michigan State University East Lansing, Michigan 48824

Received March 7, 1996; accepted August 26, 1996

Polycyclic aromatic hydrocarbons (PAHs), many of which are known carcinogens, are derived from the pyrolysis of organic materials. A rich source of PAHs is cigarette smoke, which contains methylated anthracenes and phenanthrenes as the predominant PAHs. The tumor-promoting activity of cigarette smoke has been well documented. The down-regulation of gap junction intercellular communication (GJIC) by nongenotoxic chemicals and several oncogenes has been implicated in tumor promotion. Therefore, we determined the effects of the three isomers of methylanthracene on GJIC in WB-F344 rat liver epithelial cells. Anthracene and 2-methylanthracene did not significantly inhibit GJIC, whereas anthracene methylated in the 1 or 9 position reversibly inhibited GJIC with I50 values of 22 and 36 µM, respectively. Inhibition occurred within 15 min. In conclusion, the biological effect of methylanthracene depends on the ring position of the methyl group, and these inhibitory isomers could play a potential role in tumor promotion of methylated PAH-rich mixtures such as cigarette smoke and crude oil products.


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