Abstract
Sister-chromatid exchanges (SCEs) were examined in cultured human lymphocytes after exposure for 1 h to aflatoxin B 1 (AFB 1), Trp-P-1, Trp-P-2, dimethylnitrosamine (DMN), diethylnitrosamine (DEN) and benzo[ a]pyrene (BP) with and without a metabolic activation system (S9 mix). With metabolic activation, all the carcinogens produced significant and dose-dependent increases in SCE frequency. However, the molar concentrations that induced a 2-fold increase in SCEs per cell over the control level were distributed over a range of more than 10 4. Without metabolic activation, AFB 1, at 10 −4 M, caused a significant increase in SCE induction, whereas the other compounds caused little or no increase in SCE frequency above the control levels.
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