Role of free radicals in the pathogenesis of acute chest syndrome in sickle cell disease

Acute chest syndrome (ACS) of sickle cell disease (SCD) is characterized pa thologically by vasoocclusive processes that result from abnormal interacti ons between sickle red blood cells (RBCs), white blood cells (WBCs) and/or platelets, and the vascular endothelium. One potential mechanism of vascula r damage in ACS is by generation of oxygen-related molecules, such as super oxide (O-2(-)), hydrogen peroxide (H2O2), peroxynitrite (ONOO-), and the hy droxyl (. OH) radical. The present review summarizes the evidence for alter ations in oxidant stress during ACS of SCD, and the potential contributions of RBCs, WBCs and the vascular endothelium to this process.