Journal
RESPIRATORY RESEARCH
Volume 2, Issue 5, Pages 280-285Publisher
BMC
DOI: 10.1186/rr70
Keywords
acute chest syndrome (ACS); endothelium; hemoglobin; nitric oxide (NO); oxidant stress
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Acute chest syndrome (ACS) of sickle cell disease (SCD) is characterized pathologically by vasoocclusive 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 (O-2(-)), 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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