ABSTRACT
Oxidative stress involves increased generation of free radicals, especially reactive oxygen species (ROS), and a concomitant decrease in cellular antioxidants, the major one being reduced glutathione (GSH) [7]. Factors contributing to oxidative stress in β-thalassemia are Hb-instability and iron overload [4]. The latter is caused by increased dietary iron absorption and by a failure to dispose off excess iron acquired by frequent therapeutic blood transfusions [4]. Iron participates in cellular biochemical reactions leading to generation of ROS (Fenton reaction) [8,9]. Despite extensive research on the role of oxidative stress in β-thalassemia, yielding promising results, there is a need for additional basic knowledge and for the results of preclinical and clinical trials with new antioxidants.
