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Role of free radicals in the pathogenesis of acute chest syndrome in sickle cell disease.
Respir Res. 2001; 2(5):280-5.RR

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

Klings ES
The Pulmonary Center, Boston University School of Medicine, 715 Albany Street, Boston, MA 02118, USA. eklings@lung.bumc.bu.edu
Farber HW
No affiliation info available

MeSH

Anemia, Sickle CellAnimalsAntioxidantsErythrocytesFree RadicalsHumansLeukocytesOxidantsThorax

Pub Type(s)

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

Language

eng

PubMed ID

11686897

Citation

Klings, E S., and H W. Farber. "Role of Free Radicals in the Pathogenesis of Acute Chest Syndrome in Sickle Cell Disease." Respiratory Research, vol. 2, no. 5, 2001, pp. 280-5.
Klings ES, Farber HW. Role of free radicals in the pathogenesis of acute chest syndrome in sickle cell disease. Respir Res. 2001;2(5):280-5.
Klings, E. S., & Farber, H. W. (2001). Role of free radicals in the pathogenesis of acute chest syndrome in sickle cell disease. Respiratory Research, 2(5), 280-5.
Klings ES, Farber HW. Role of Free Radicals in the Pathogenesis of Acute Chest Syndrome in Sickle Cell Disease. Respir Res. 2001;2(5):280-5. PubMed PMID: 11686897.
* Article titles in AMA citation format should be in sentence-case
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 - 2001/02/06/received PY - 2001/03/26/revised PY - 2001/05/18/accepted PY - 2001/11/1/pubmed PY - 2002/1/5/medline 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 - https://respiratory-research.biomedcentral.com/articles/10.1186/rr70 DB - PRIME DP - Unbound Medicine ER -