Abstract
The ability of trichloroacetic acid (TCA) to act as an initiator or promoter of carcinogenesis was studied in the γ-glutamyl transpeptidase (GGT) enzyme altered foci (EAF) assay, using the rat partial hepatectomy model and diethylnitrosamine (DEN) phenobarbital (PB) positive controls. The capacity of TCA to induce peroxisomal proliferation was examined by measuring the induction of hepatic peroxisomal-dependent14C-palmitoyl-CoA. Induction of hepatic ornithine decarboxylase (ODC) was also measured.
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