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

Published by National Institutes of Health | U.S. Department of Health & Human Services | Catalog Last Checked: July 31, 2026 at 09:56 PM | Dataset Last Updated: September 06, 2025
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.

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