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

Abstract

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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  • Authors+Show Affiliations

    ,

    The Pulmonary Center, Boston University School of Medicine, 715 Albany Street, Boston, MA 02118, USA. eklings@lung.bumc.bu.edu

    Source

    Respiratory research 2:5 2001 pg 280-5

    MeSH

    Anemia, Sickle Cell
    Animals
    Antioxidants
    Erythrocytes
    Free Radicals
    Humans
    Leukocytes
    Oxidants
    Thorax

    Pub Type(s)

    Journal Article
    Research Support, Non-U.S. Gov't
    Review

    Language

    eng

    PubMed ID

    11686897

    Citation

    TY - JOUR T1 - Role of free radicals in the pathogenesis of acute chest syndrome in sickle cell disease. AU - Klings,E S, AU - Farber,H W, Y1 - 2001/07/13/ PY - 2001/11/1/pubmed PY - 2002/1/5/medline PY - 2001/Feb/6/received PY - 2001/Mar/26/revised PY - 2001/May/18/accepted PY - 2001/Jul/13/aheadofprint PY - 2001/11/1/entrez SP - 280 EP - 5 JF - Respiratory research JO - Respir. Res. VL - 2 IS - 5 N2 - 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. SN - 1465-9921 UR - https://www.unboundmedicine.com/medline/citation/11686897/full_citation L2 - http://www.biomedcentral.com/1465-9921/2/280 ER -