Title: The effects of anthracene and methylated anthracenes on gap junctional intercellular communication in rat liver epithelial cells.

Authors: Upham, B L; Weis, L M; Rummel, A M; Masten, S J; Trosko, J E

Published In Fundam Appl Toxicol, (1996 Dec)

Abstract: 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 microM, 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.

PubMed ID: 8954755

MeSH Terms: Animals; Anthracenes/toxicity*; Cell Communication/drug effects*; Cell Survival/drug effects; Cells, Cultured; Down-Regulation/drug effects; Epithelial Cells; Epithelium/drug effects; Gap Junctions/drug effects*; Liver/cytology*; Liver/drug effects*; Methylation; Rats; Rats, Inbred F344; Structure-Activity Relationship