**1. Introduction**

Iron is an essential trace element found in all cellular forms of life and plays a crucial role in oxygen sensing and transport, electron transfer, and catalysis [1]. In ancient times, iron was used in medicine for the treatment of the following diseases; alopecia, acne, vesicular bollus, encrusting eruptions, erysipelas, paronychia, vaginal discharges, wounds, hemorrhoids, gout, tuberculosis, diarrhea, perianal fistulas, excessive lacrimation, vomiting, weakness, edema, fevers and cystitis [2]. Secondary iron overload in β-thalassemia patients is commonly caused by increased dietary iron absorption and can be a result of multiple blood transfusions [3]. Consequently, the excessive active iron catalyzes the production of a variety of reactive oxygen species (ROS), such as superoxide anions (O2 •-), hydrogen peroxide (H2O2) and hydroxyl radicals (HO•) via Haber-Weiss and Fenton reactions. The ROS is attributed to the function of the metal in the redox cycle and can damage many cells and tissues including the heart, liver, pancreas, erythrocytes and endocrine glands resulting in dysfunctions of the organs [4]. Hydrogen peroxide is normally applied to kill microorganisms in neutrophils; nevertheless, an excess amount can be toxic.

β-Thalassemia patients suffer from ineffective erythropoiesis and require regular blood transfusions to compensate for having chronic anemia. Transfused red blood cells (RBC) are taken up and degraded by the reticuloendothelial system (RES) or tissue macrophages, leading to a high accumulation of intracellular iron and saturation of plasma transferrin. The excess iron appears in successive forms of toxic iron as a labile iron pool (LIP), and non-transferrin bound iron (NTBI) and labile plasma iron (LPI) [5-7]. Effective iron chelators are required to remove the toxic irons in order to prevent oxidative damage in the vital organs, particularly the heart and liver. Iron chelators must be absorbed via the gastrointestinal tract into the blood circulation and target tissues readily, and show minimal side effects. They should complex

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directly onto the plasma iron as well as the cellular iron; afterwards, the complexes can be excreted from the body easily [8]. Serum oxidant activity in young β-thalassemia major patients with iron overload is directly correlated with the serum ceruloplasmin and copper concentra‐ tions, and with serum iron (SI) concentration and total iron-binding capacity (TIBC), but not with serum vitamin E concentration [9]. Levels of antioxidant enzymes such as superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx) were greatly elevated in the RBC of β-thalassemia minor patients to fight cellular increased oxidant and are close to normal values in the RBC of β-thalassemia major patients due to the presence of transfused normal RBC [10]. Levels of antioxidant compounds such as serum retinol (vitamin A), carotenoids, α-tocopherol (vitamin E) were decreased in β-thalassemia major patients [11, 12]. Supplements of the antioxidant vitamins can prevent some of the damage in the thalassemic RBC membrane. Thus, antioxidant therapy can be a supplemental medical regime to meliorate pathophysiological complications and improve quality of life of thalassemia patients.
