Peroxidative stress and antioxidant enzymes in children with beta-thalassemia major

Regular blood transfusions and secondary iron overload make thalassemic erythrocytes prone to peroxidative injury. Although some reports suggest endogenous free radical damage in thalassemia, there remains discrepancy in the status of antioxidant enzymes. The aim of this study was to evaluate the extent of lipid peroxidation and status of antioxidant enzyme in children with beta-thalassemia.

Fifty transfusion-dependent beta-thalassemics were subjected to analysis of lipoperoxides as malondialdehyde (MDA), nitric oxide (NOx), superoxide dismutase (SOD), glutathione (GSH), and glutathione peroxidase (GPx) along with serum iron and ferritin, liver functions and uric acid. Plasma MDA was analyzed to indicate the oxidative parameters, whereas the erythrocyte SOD, GPx, and plasma NOx were measured to show the antioxidant status of the children. All these parameters in 30 non-anemic healthy controls attending the child health promotion clinic of hospital were also studied.

All the patients were iron overloaded. Markers of free radical injury such as MDA and antioxidant enzyme SOD and NOx levels were significantly elevated in thalassemic children while mean GPx levels were decreased in patients compared to controls (P < 0.001). All these markers significantly correlated with serum ferritin levels. There was no significant difference in levels of GSH measured but it correlated with serum iron levels.

Our study results suggest that iron overload causes peroxidative damage in beta-thalassemia and antioxidant systems try to compensate for reducing lipid peroxidation to lower tissue damage.