Figure 6.

Schematic model of cytoprotective mechanisms in response to oxidative stress in β-thalassemic erythroid cells. In β-thalassemic erythropoiesis ROS inhibits 5-δ aminolevulinate synthase (ALAS-2) activity, reducing the neosynthesis of heme, and induces peroxiredoxin-2 (PRDX2) expression. In the early stage of β-thalassemic eythropoiesis, ROS and heme levels are both increased and PRDX2 acts on both targets; in more mature cells, when ROS levels are still high and heme levels are reduced, ROS might become the PRDX2 major target (see text for details).