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.
Klings
E S
ES
The Pulmonary Center, Boston University School of Medicine, 715 Albany Street, Boston, MA 02118, USA. eklings@lung.bumc.bu.edu
Farber
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HW
D000755:Anemia, Sickle Cell / Q000097:blood / Q000150:complications* / Q000503:physiopathology; D000818:Animals; D000975:Antioxidants / Q000378:metabolism; D004912:Erythrocytes / Q000378:metabolism; D005609:Free Radicals / Q000097:blood*; D006801:Humans; D007962:Leukocytes / Q000378:metabolism; D016877:Oxidants / Q000097:blood; D013909:Thorax / Q000502:physiology
D000975:Antioxidants; D005609:Free Radicals; D016877:Oxidants