THE EFFECTS OF ANTHRACENE AND METHYLATED ANTHRACENES ON GAP JUNCTIONAL INTERCELLULAR COMMUNICATION IN RAT-LIVER EPITHELIAL-CELLS

Polycyclic aromatic hydrocarbons (PAHs), many of which are known carci nogens, are derived from the pyrolysis of organic materials. A rich so urce of PAHs is cigarette smoke, which contains methylated anthracenes and phenanthrenes as the predominant PAHs. The tumor-promoting activi ty of cigarette smoke has been well documented. The down-regulation of gap junction intercellular communication (GJIC) by nongenotoxic chemi cals and several oncogenes has been implicated in tumor promotion. The refore, we determined the effects of the three isomers of methylanthra cene on GJIC in WB-F344 rat liver epithelial cells. Anthracene and 2-m ethylanthracene did not significantly inhibit GJIC, whereas anthracene methylated in the 1 or 9 position reversibly inhibited GJIC with I-50 values of 22 and 36 mu M, 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 isomer s could play a potential role in tumor promotion of methylated PAH-ric h mixtures such as cigarette smoke and crude oil products. (C) 1996 So ciety of Toxicology.