The role of oxidant damage to red cells in sickle cell anemia has been of interest in recent years. The generation of reactive oxygen species is a steady-state cellular event in respiring cells. Their production can be grossly amplified in response to a variety of pathophysiological conditions such as inflammation, immunologic disorders, hypoxia, hyperoxia, metabolism of drugs or alcohol, exposure to UV or therapeutic radiation, and deficiency in antioxidants enzymes [
12]. SCD is a hereditary disorder with higher potential for oxidative damage due to chronic redox imbalance in red cells that often results in clinical manifestation of mild-to severe hemolysis in patients with this genetic disorder [
13]. It was shown that SS patients produced greater quantities of O
2−, H
2O
2 and OH
· than AA patients with normal red blood cells [
14]. The present study investigated the variation between pro and antioxidant markers of the homozygote sickle and healthy patients and the results showed that the activities of SOD, CAT, NO and TAC were significantly decreased in the SS subjects as compared with the control normal subject group AA. The deficiency of the activities of these enzymes may be attributed to the high production of ROS in these patients which may destroy these antioxidant enzymes [
2]. Some previous studies demonstrated that the activities of SOD, CAT and peroxidase were reduced while others reported that the activities of both SOD and peroxidase were increased [
15,
16]. The decrease of the levels of SOD in the sickle patients as found in this study could be able to increase the flux of superoxide ion exposing the sickle erythrocytes to high level of hydrogen peroxide. Furthermore, the increase of MDA in the same group can be attributed to the auto-oxidation of iron seen in these patients [
15]. Also, the excess production of MDA has additional toxic effects leading to alterations of the proteins, modifications of amino-acid side chain, and lipids structure. These alterations may result in a partial or complete loss of protein functionality including antioxidant enzymes, protein receptors [
2,
17] and cause externalization of phosphatidylserine in red cell membranes which can enhance complement activation and cell lysis [
12].
The data showed that except for MDA, there was an increase of the remaining oxidative stress markers tested in both females SS and healthy patients. Difference between males and females in this study may also be due to the fact that women have a source of antioxidant protection (oestrogen) which is low or absent in men [
18]. Previous study demonstrated similar results [
19]. MDA, which is major aldehyde product of lipid peroxidation, reflects damage to lipids. Many studies support the role of estrogens in the primary and secondary prevention of Cardiovascular Disease (CVD) among women, particularly in normalizing blood lipids or inducing endothelium-dependent vasodilation stimulating nitric oxide synthetase [
20]. The severe alteration of the oxidative pattern in the male homozygote SS may offer one possible pathogenetic explanation for the higher incidence of crisis and complications observed in SS males than females.