BACKGROUND/AIMS: Lipid peroxidation/oxidative stress and/or endotoxin-induced cytokine release are implicated in the non-alcoholic fatty liver disease pathogenesis. Studies in the literature are experimental in nature and are based on histopathological evaluation and peripheral blood findings. In this study, we aimed to investigate the relationships between lipid peroxidation and antioxidant capacity in non-alcoholic fatty liver disease. METHODS: Twenty-six patients with an ethanol consumption of less than 20 g/day who were diagnosed ultrasonographically and histopathologically as non-alcoholic fatty liver disease and 16 healthy control subjects with normal ultrasonographical findings were included in the study. All viral and autoimmune markers in patient and control groups included in the study were negative. Non-alcoholic steatohepatitis samples obtained by fine needle aspiration were evaluated according to Brunt et al. The levels of glutathione, catalase, superoxide dismutase, and malonyldialdehyde in peripheral blood and liver biopsy samples were measured. RESULTS: Of patients with non-alcoholic fatty liver disease, 17 (65%) were detected to have mild, 7 (27%) moderate and 2 (8%) severe steatosis; portal inflammation was found in 17 patients (65%) and stage I fibrosis in 21 patients (80%). Minimal lobular inflammation was observed in all patients. In the patient group, the levels of erythrocytic glutathione, catalase, and superoxide dismutase were significantly lower but malonyldialdehyde levels were higher compared to the control group. It was revealed that hepatocytic reduced glutathione, catalase, and malonyldialdehyde levels were not correlated with peripheral blood levels, but there was a positive correlation between liver malonyldialdehyde level and liver reduced glutathione level. Plasma malonyldialdehyde level and liver glutathione had a negative correlation. CONCLUSIONS: It was discovered that lipid peroxidation and antioxidant capacity suppression due to its overuse were important in the non-alcoholic fatty liver disease pathogenesis, but antioxidant capacity was maintained well at tissue level in the early stages of the disease. Furthermore, it was identified that tissue lipid peroxidation and changes in antioxidant capacity were not reflected in the peripheral blood to the same extent.
BACKGROUND/AIMS: Lipid peroxidation/oxidative stress and/or endotoxin-induced cytokine release are implicated in the non-alcoholic fatty liver disease pathogenesis. Studies in the literature are experimental in nature and are based on histopathological evaluation and peripheral blood findings. In this study, we aimed to investigate the relationships between lipid peroxidation and antioxidant capacity in non-alcoholic fatty liver disease. METHODS: Twenty-six patients with an ethanol consumption of less than 20 g/day who were diagnosed ultrasonographically and histopathologically as non-alcoholic fatty liver disease and 16 healthy control subjects with normal ultrasonographical findings were included in the study. All viral and autoimmune markers in patient and control groups included in the study were negative. Non-alcoholic steatohepatitis samples obtained by fine needle aspiration were evaluated according to Brunt et al. The levels of glutathione, catalase, superoxide dismutase, and malonyldialdehyde in peripheral blood and liver biopsy samples were measured. RESULTS: Of patients with non-alcoholic fatty liver disease, 17 (65%) were detected to have mild, 7 (27%) moderate and 2 (8%) severe steatosis; portal inflammation was found in 17 patients (65%) and stage I fibrosis in 21 patients (80%). Minimal lobular inflammation was observed in all patients. In the patient group, the levels of erythrocytic glutathione, catalase, and superoxide dismutase were significantly lower but malonyldialdehyde levels were higher compared to the control group. It was revealed that hepatocytic reduced glutathione, catalase, and malonyldialdehyde levels were not correlated with peripheral blood levels, but there was a positive correlation between liver malonyldialdehyde level and liver reduced glutathione level. Plasma malonyldialdehyde level and liver glutathione had a negative correlation. CONCLUSIONS: It was discovered that lipid peroxidation and antioxidant capacity suppression due to its overuse were important in the non-alcoholic fatty liver disease pathogenesis, but antioxidant capacity was maintained well at tissue level in the early stages of the disease. Furthermore, it was identified that tissue lipid peroxidation and changes in antioxidant capacity were not reflected in the peripheral blood to the same extent.