Differential inducibility of chromosome aberrations and sister-chromatid exchanges by indirect mutagens in various mammalian cell lines.

A total of 17 cultured mammalian cell lines of various types was investigated for the inducibility of chromosome aberrations (CAs) and sister-chromatid exchanges (SCEs) after exposure to 3 direct mutagens, cyclophosphamide (CP), dimethylnitrosamine (DMN) and benzo[a]pyrene (BP), without extrinsic metabolizing factors. The following cell lines were highly sensitive to CP as estimated by the dose-dependent increase of either CAs or SCEs, or both: 4 rat ascites hepatomas (AH66-B, AH66-C, AH70B, AH109A), 3 rat esophageal tumors (R1, R2, R3), the Yoshida sarcoma (YS), a Chinese hamster embryonic cell line (B-13), and a human embryonic (HE2236) cell line. 1 golden-hamster embryonic (GHE), 1 human embryonic (HE2144) and 1 human esophageal tumor (TH) cell line were moderately sensitive to CP in terms of the yield of SCEs, though they showed rather low sensitivity when measured by the frequency of CAs. 2 Chinese hamster (CHO-K1, CHL) and 1 human lymphoma (P3HR-1) cell lines were much less sensitive or almost insensitive with respect to the yield of both CAs and SCEs. Considering the above results and taking some other experimental conditions into account, 7 cell lines, including another Chinese hamster cell line (Don 6), were similarly investigated with DMN and BP. The results indicated that AH66-B, which was highly sensitive to CP, was also sensitive to DMN and BP, and that the CP-sensitive R1 and R3 were responsive to DMN. While YS, B-13, Don 6 and P3HR-1 did not show any significant response to DMN, a considerable increment of SCEs was noted in B-13 after treatment with BP, GHE was also notable for its high sensitivity to BP, showing an apparently dose-dependent increase of both CAs and SCEs. HE2144 exhibited a slightly increased rate of SCEs after exposure to BP.