Resistance of Erythrocytes to Lipid Peroxidation in Cirrhotic Rats

Background m of the present study was to investigate erythrocyte prooxidant−antioxidant balance in relation to liver and plasma lipid peroxidation in thioacetamide (TAA)-induced liver cirrhosis in rats. s cirrhosis was produced by the administration of TAA (0.3 g/L of tap water) for a period of 3 months in rats. Serum, liver and erythrocyte lipid peroxide levels as well as liver glutathione (GSH) levels and superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) activities were determined in cirrhotic rats. s c cirrhosis was assessed by biochemical and histopathological findings. Serum alanine transaminase (ALT) and aspartate transaminase (AST) activities and malondialdehyde (MDA) levels increased in cirrhotic rats. This treatment caused increased MDA and diene conjugate (DC) levels as well as decreased GSH levels and GSH-Px activities in the liver of cirrhotic rats. In these conditions, no significant changes in erythrocyte cholesterol, phospholipid levels as well as endogenous DC, and GSH levels and spontaneous hemolysis values were observed in erythrocytes of rats with TAA-induced liver cirrhosis. However, H2O2-induced MDA levels were detected to decrease significantly in erythrocytes of cirrhotic rats. sions sults indicate that erythrocytes of TAA-induced cirrhotic rats have a resistance against peroxidative stress in contrast to the findings in plasma and liver.