Induction of sister-chromatid exchanges by direct and indirect agents in a human teratoma cell line.

We have extended the characterization of the P3 cell line, derived from a human epithelial teratocarcinoma, by studying the induction of sister-chromatid exchanges (SCEs) by direct and indirect carcinogens. Several direct acting carcinogens produce a dose-dependent increase in SCEs. Most notably, N-methyl-N'-nitro-N-nitrosoguanidine and 7 beta,8 alpha-dihydroxy-9 alpha,10 alpha-epoxy-7,8,9,10-tetrahydrobenzo[a]pyrene produce increases in SCEs at doses comparable to those used to induce mutations at the hypoxanthine-guanine phosphoribosyl transferase locus. The indirect carcinogens elicit SCEs only when the P3 cells are cocultured with cells capable of metabolizing the indirect carcinogens to the active form. Human breast carcinoma (BJ-015) and rat hepatoma (RL-12) cells are equally efficient in activating polycyclic aromatic hydrocarbons to the active form. This cell-mediated induction of SCEs is obtained when the P3 cells are incubated with live, X-irradiated, or UV-irradiated BJ or RL cells. This P3 cell line is thus equally suitable to study the induction of mutations or the induction of SCEs with direct and indirect carcinogens.