Superoxide Dismutase and Lipid Peroxidation in Acute Lymphocytic Leukemia

Abstract

There is much evidence suggesting a possible role of reactive oxygen species and other free radicals as mediators of phenotypic and genotypic changes that lead from mutation to cancer. The imbalance in cancer cell antioxidant defense mechanism can influence also the sensitivity to cytoreductive therapy. In erythrocytes, it can result in hemolysis which is one of the pathogenic mechanisms of anemia in cancer patients. Parameters of lipid peroxidation (malondialdehyde, MDA) and antioxidant enzymes here represented by superoxide dismutase (SOD) have been investigated in acute lymphocytic leukemia. Twenty patients of various stages and activities of the disease and twenty five normal controls were recruited. Significantly higher concentrations of total MDA in plasma (28.10 ± 2.90 nmol/L vs. 9.20 ± 0.30 nmol/L, p < 0.0001) as well as in erythrocytes (3.00 ± 0.20 nmol/gHb vs. 1.20 ± 0.10 nmol/gHb, p < 0.0001) were found compared to the control group. Significantly lower activity of SOD (1,966 ± 110 U/gHb vs. 3,095 ± 60 U/gHb, p < 0.0001) was also observed. No correlations were obtained between SOD activity, MDA concentration in both red cells and plasma with blast cell count and hemoglobin concentration. This study suggests that free radicals are associated with an impaired antioxidant defense enzyme activity resulting in increased lipid peroxidation in acute lymphocytic leukemia.