The role of oxidant injury in the pathophysiology of human thalassemias

Stanley L. Schrier, Filippo Centis, Michael Verneris, Lisa Ma, Emanuele Angelucci

Research output: Contribution to journalArticlepeer-review

43 Scopus citations

Abstract

The anemia in β-thalassemia major is caused by a combination of hemolysis and ineffective erythropoiesis, with the latter being more important. Studies of the underlying cause of the hemolysis have indicated that oxidant injury to circulating red blood cells (RBCs) was of critical importance, with evidence of oxidant damage to RBC membrane proteins 4.1 and band 3. Therefore, it seemed reasonable that oxidant damage to thalassemic erythroid precursors would cause their accelerated apoptosis and ineffective erythropoiesis. However, direct analysis showed that the apoptotic programs turned on in thalassemics were not those triggered by oxidative damage but were dependent on activation of FAS/FAS-Ligand interaction. Thus, destruction of thalassemic erythroid precursors may involve different mechanisms from those that cause RBC hemolysis.

Original languageEnglish (US)
Pages (from-to)241-245
Number of pages5
JournalRedox Report
Volume8
Issue number5
DOIs
StatePublished - 2003

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