Murison G L
Department of Biological Sciences, Florida International University, Miami 33199.
Mutat Res. 1988 Oct;203(5):347-54. doi: 10.1016/0165-1161(88)90031-3.
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.
我们通过研究直接致癌物和间接致癌物对姐妹染色单体交换（SCEs）的诱导作用，扩展了对源自人上皮性畸胎癌的P3细胞系的特性描述。几种直接作用的致癌物会使SCEs呈剂量依赖性增加。最值得注意的是，N-甲基-N'-硝基-N-亚硝基胍和7β,8α-二羟基-9α,10α-环氧-7,8,9,10-四氢苯并[a]芘在与用于诱导次黄嘌呤-鸟嘌呤磷酸核糖基转移酶位点突变的剂量相当的情况下，会使SCEs增加。只有当P3细胞与能够将间接致癌物代谢为活性形式的细胞共培养时，间接致癌物才会引发SCEs。人乳腺癌（BJ-015）细胞和大鼠肝癌（RL-12）细胞在将多环芳烃激活为活性形式方面同样有效。当P3细胞与活的、经X射线照射或紫外线照射的BJ或RL细胞一起孵育时，可获得这种细胞介导的SCEs诱导。因此，这种P3细胞系同样适合用于研究直接致癌物和间接致癌物诱导的突变或SCEs。
