Deferasirox: Oral, once daily iron chelator - An expert opinion.

Iron overload is a serious and potentially fatal condition that results from multiple blood transfusions required over a long period of time to treat certain types of anemias such as, that caused by β-thalassemia, sickle cell disease and myelodysplastic syndrome. Deferoxamine, which has been used since four decades as an iron chelator has limited efficacy due to its demanding therapeutic regimen, leading to poor compliance. Deferasirox, once daily oral iron chelator provides an effective alternative to Deferoxamine in the treatment of transfusional hemosiderosis. In this review, the role of Deferasirox as an ideal iron chelator has been discussed. Pubmed searches on Deferasirox were carried out for the same. Several studies demonstrated the safety and efficacy of Deferasirox in reducing iron burden in iron-overloaded patients with β-thalassemia, sickle cell anemia and myelodysplastic anemia. Thus, convenient, effective and tolerable chelation therapy with oral Deferasirox is likely to be a significant development in the treatment of transfusional iron overload, due to its ability to provide constant chelation coverage and the potential to improve compliance.

Oxidative damage of DNA and benzoate by chelated and non-chelated copper in presence of hydrogen peroxide.

Benzoate hydroxylation test revealed that Cu(II) reacting with H2O2 produced OH degree radicals, which nicked or damaged DNA or hydroxylated benzoate, the extent of damage or hydroxylation depending on the period of incubation. The production of OH degree free radicals was also supported by the scavenger studies. Neither Cu(II) nor H2O2 alone could damage DNA or hydroxylate benzoate. EDTA-chelated Cu(II) plus H2O2 could damage DNA or hydroxylate benzoate only in presence of the biological reductant, L-cysteine, the damage increased with the increasing molar ratio of L-cysteine to Cu-EDTA. The biological relevance of the EDTA chelated Cu(II) and H2O2 system is discussed.