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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 pathologically by vaso-occlusive processes that result from abnormal interactions between sickle red blood cells (RBCs), white blood cells (WBCs) and/or platelets, and the vascular endothelium. One potential mechanism of vascular damage in ACS is by generation of oxygen-related molecules, such as superoxide (O2-), hydrogen peroxide (H2O2), peroxynitrite (ONOO-), and the hydroxyl (*OH) radical. The present review summarizes the evidence for alterations in oxidant stress during ACS of SCD, and the potential contributions of RBCs, WBCs and the vascular endothelium to this process.
The Pulmonary Center, Boston University School of Medicine, 715 Albany Street, Boston, MA 02118, USA. email@example.com
MeSHAnemia, Sickle Cell
Pub Type(s)Journal Article
Research Support, Non-U.S. Gov't