The effects of two hepatocarcinogens, 1,1,1-trichloro-2,2-di-4-(chlorophenyl)ethane and 1,1-dichloro-2,2-bis(p-chlorophenyl)ethylene (DDT and DDE), on hepatic biochemical parameters were examined in adult female rats and mice. Two oral administrations of DDT (66 mg/kg) at 21 and 4 hr before sacrifice increased rat hepatic microsomal cytochrome P-450 content by 28%. After two oral treatments with 175 and 525 mg/kg 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 activity was not elevated above control values. Neither DDT nor DDE caused any significant biochemical changes in mouse liver. Thus rat hepatic ODC, a biochemical marker for tumor-promoters, responded to DDE, the stronger of the two hepatocarcinogens, but not to DDT. Neither DDT nor DDE caused hepatic DNA damage in either rat or mouse liver.