ABSTRACT
Disturbance of the balance between the production of reactive oxygen species [ROS] and antioxidant defenses against them produces oxidative stress which amplifies tissue and DNA damage leading to mutagenesis, carcinogenesis and cell death. This study was undertaken to examine the role of treatment with hepanox, a commercially antioxidant, with a dose of 0.3 capsule/kg body weight/day on oxidatiuve stress and antioxidant defense methanisms on rats bearing hepatocellular carcinoma [HCC] induced by nitrosamine precurors. The activities of both blood and serum superoxide dismutase [SOD] and blood catalase, glutathione reductase [GSH-R] and glutathione peroxidase [GSH- Px] as well as the levels of glutathione [GSH], malondialdhyde [MDA] and liver tissue DNA in addition to the parameters of liver function tests [LFTs] were studied in 4 groups of 10 rats each. HCC occurs only after 7 months of nitrosamine precursors intake which was characterized by architectural and cellular damage of hepatic lubules and hepatocytes as well as increase in the levels of DNA [P<0.01]. These structrural changes were accompanied by hyperbilirubinemia, hypoalbuminemia and increase in the activities of transaminases [P<0.01]. The causative factors of these disturbances may be due to the imbalance between the activities of both GSH-R and GSHPx which result iii reduction of GSH with the increase in the duration of hepatocarcinogenic intake [P<0.01 ]. In addition, a balance between the activities of these enzymes resulted in relevation of GSH, reduction of liver DNA and blood MDA mean levels as well as normalization of LFTs in animal groups intaken hepanox and nitrosamine precursors or those intaken hepanox only as a result of controlling the process of lipid peroxidation [P<0.001]. Furthermore, the mechanisms of the protective effects of hepanox via its contents of zinc, vitamin E and sylimarin were discussed. These findings intense more light on the protective effects of hepanox, as an antioxidants containing drug, at least in part on LETs of patients with liver damage