Background - The role of selenium, in the form of selenomethionine-supplemented drinking water (0.008 g/l), in inhibiting hepatocarcinogenesis induced by 2-acetylaminofluorene (0.05% in the basal diet) in Sprague Dawley male rats was evaluated. Methods - Selenomethionine treatment before initiation, during initiation and during the selection/promotion phases of hepatocarcinogenesis was studied. The study was extended to investigate and correlate lipid peroxidation, cellular protein damage, hemoglobin status in erythrocytes and liver microsomal gamma-glutamyl transferase during the initiation and promotion stage[s] of hepatocarcinogenesis. Results - Selenomethionine administration altered lipid peroxidation (67% reduction), proteolysis (66% reduction), hemoglobin content (60% increase), percentage of methemoglobin (2-fold increase), percentage of hemolysis (about 50% reduction) in blood as well as the activity of gamma-glutamyl transferase in nodules/hepatoma (74% reduction) and non-nodular surrounding parenchymal tissue (51% reduction) in the liver during the long-term initiation study, as compared with carcinogen controls, and contributed towards a delay of hepatocarcinogenesis induced by chronic exposure to 2-acetylaminofluorene. Conclusions - Selenomethionine is not only able to reduce the activity of the hepatic preneoplastic marker enzyme gamma-glutamyl transferase, but also improves hematological markers in terms of better protection and stabilization of erythrocytes during hepatocarcinogenesis induced by 2-acetylaminofluorene. Our results confirm that the inhibitory effect of selenomethionine is primarily exerted on the initiation phase of the hepatocarcinogenic process. Nevertheless, a continuous long-term exposure confers a greater degree of protection.
