The effects of long-term administration of tocotrienol on hepatocarcinogenesis in rats induced by diethylnitrosamine (DEN) and 2-acetylaminofluorene (AAF) were investigated by determining the activities of gamma-glutamyl transpeptidase (GGT), alkaline phosphatase (ALP), glutathione S-transferases (GSTs), and glutathione (GSH) levels in blood and liver. Twenty-eight male 7- to 8-wk-old Rattus norwegicus rats, weighing 120-160 g, were used in this study. The rats were divided into four treatment groups: a control group on a basal diet, a group fed a basal diet supplemented with tocotrienol (30 mg/kg food), a group treated with DEN/AAF, and a group treated with DEN/AAF and fed a diet supplemented with tocotrienol (30 mg/kg food). Blood was collected monthly, and GGT, ALP, and GSH levels were determined. The rats were killed after 9 mo, and the livers were examined morphologically. Grayish white nodules (2/liver) were found in all the DEN/AAF-treated rats (n = 10), but only one of the rats treated with DEN/AAF and supplemented with tocotrienol (n = 6) had liver nodules. A significant increase in the level of blood and liver GSH, ALP, and GGT activities was observed in the DEN/AAF-treated rats. Liver GSTs were similarly increased with DEN/AAF treatment. Tocotrienol supplementation attenuated the impact of the carcinogens in the rats.
An attempt was made to clarify the association between zinc (Zn) and antioxidants due to Zn supplementation on lipid peroxidation occurring during Brachiaria decumbens intoxication. The concentration of Zn, copper, malondialdehyde (MDA), superoxide dismutase (SOD), and gluthathione peroxidase (GSH-Px) were determined in tissues. There was a gradual increment in the concentration of Zn and MDA in serum and hepatocytic SOD in groups given Zn + B decumbens. A decline in erythrocytic GSH-Px and SOD, and lower concentration of reduced glutathione in hepatocyte cytosols were also detected in these sheep. It is highly suggestive that Zn supplementation may depress antioxidant status and enhance lipid peroxidation during B decumbens intoxication.