The effects of two hepatocarcinogens (DDT and DDE) on hepatic biomedical parameters were examined in adult female rats and mice. Two oral administrations of DDT (66 mg/kg/day) at 21 and 4 hours before sacrifice increased rat hepatic microsomal cytochrome P-450 content by 28%. After two oral treatments with 175 and 525 mg/kg/day of DDE, rat hepatic ornithine decarboxylase (ODC) activity was increased 6.5 and 22 fold while cytochrome P-450 content was elevated by 58% and 123% respectively. As DDT did not acutely increase rat ODC activity, a chronic exposure to DDT was also performed. Thirty days after a single oral treatment with 90 mg/kg DDT, rat hepatic ODC was not elevated above control values. Neither DDT or DDE caused any significant biochemical changes in mouse liver. Thus rat hepatic ODC, a biochemical marker for carcinogenic promotional potential, responded to DDE, the stronger of the two hepatocarcinogens, but not to DDT. Neither DDT or DDE caused hepatic DNA damage in either rat or mouse liver.