BETA-CAROTENE PREVENTS LIPID-PEROXIDATION AND RED-BLOOD-CELL MEMBRANE-PROTEIN DAMAGE IN EXPERIMENTAL HEPATO CARCINOGENESIS

The anti-cancer efficacy of dietary beta-carotene (BC, 120 mg/kg diet, daily) was evaluated during diethylnitrosamine (DEN, 200 mg/kg body w eight)-induced hepatocarcinogenesis in male Sprague-Dawley rats. BC tr eatment was carried out throughout the study, before initiation or sel ection/promotion phase of hepatocarcinogenesis in a defined experiment al protocol. In red blood cells (RBC) and microsomal fractions from he patic nodular and non-nodular surrounding parenchyma, the enzymatic li pid peroxidation increased significantly by more than 3-fold, 9- to 10 -fold and 4- to 7-fold respectively 18 weeks following initiation by D EN as compared to normal control animals, RBC membrane protein damage was estimated by alanine release and was found to increase more than 5 -fold in the same time period in DEN control rats. A decrease in hepat ic cytosolic and microsomal glucose-6-phosphatase activities was obser ved, whereas the activities of the oxygen-derived free-radical scaveng er enzymes, like cytosolic catalase and superoxide dismutase, were sho wn to increase significantly at the same time point. However, BC expos ure in the different phases of hepatocarcinogenesis substantially chan ged all the above parameters in limiting the action of DEN. Results sh owed that the most significant beneficial effect of BC during hepatoca rcinogenesis was exerted mainly in long term continuous and/or the ini tiation phase of carcinogenicity, rather than in the selection/promoti on phase. Moreover, the volumetric and numerical densities of the pren eoplastic lesions were all appreciably reduced by exposure to BC. We c onclude that Long term intake of BC could reduce cancer risk by preven ting hepatic lipid peroxidation and RBC membrane protein damage due to its antioxidant actions.