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Title: Role of antioxidant and iron chelating therapies in Thalassemia patients
Authors: Ruchaneekorn W. Kalpravidh
Suneerat Hatairaktham
Mahidol University
Keywords: Medicine
Issue Date: 1-Dec-2012
Citation: Handbook on Oxidative Stress New Research. (2012), 329-346
Abstract: Thalassemia could be regarded as an "oxidative stress" disorder because its pathogenesis inevitably contributes to anemia and iron overload conditions, typically leading to oxidative damage of cells and organs in the patients. Over decades, alleviation strategies of iron-induced oxidative stress, either by antioxidant supplementation or iron chelation, have been extensively studied. Although antioxidants are not able to increase hemoglobin concentration, they exert preventive effects by direct scavenging of free radicals, modulating gene expression of proteins involved in oxidative cascade, up-regulating the activities of cellular antioxidant enzymes, and chelating metal ions. The iron toxicity is mainly caused by non-transferrin bound iron (NTBI) formed after transferrin saturation which is highly reactive and uncontrollable uptake into cells. During iron-chelating programs, the decreased levels of serum ferritin and NTBI, and the clearance of iron loaded in various organs such as heart, liver, and endocrine glands have been reported with variable degree of efficacy and side effects. In this article, we summarize the central role of oxidative stress in thalassemia pathogenesis and also discuss the therapeutic effects of potential antioxidants such as vitamin E, curcuminoids, catechins, and coenzyme Q10 based on emerging data from several animal studies and clinical trials. Furthermore, the importance of iron chelators is also highlighted. Finally, the concept of combined therapies between antioxidants and iron chelators has been evaluated with the goal to reduce side effects and increase treatment efficacy, which results in improved quality of life and increased life expectancy in the iron-overloaded thalassemia patients. © 2012 Nova Science Publishers, Inc.
Appears in Collections:Scopus 2011-2015

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