Journal
AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE
Volume 164, Issue 7, Pages 1248-1252Publisher
AMER THORACIC SOC
DOI: 10.1164/ajrccm.164.7.2101020
Keywords
hemoglobin; lung disease; reactive oxygen species; nitric oxide
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Funding
- NCI NIH HHS [IP030 CA68485] Funding Source: Medline
- NHLBI NIH HHS [R01-HL55198] Funding Source: Medline
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Nitric oxide metabolism is altered during the acute chest syndrome of sickle cell disease. In the presence of oxygen and oxygen-related molecules, nitric oxide can preferentially form the powerful oxidants nitrite, nitrate, and peroxynitrite. We hypothesized that increased oxidative stress may contribute to the pathogenesis of acute chest syndrome and measured F-2 isoprostanes, a nonenzymatically generated molecule resulting from free radical catalyzed lipid peroxidation in patients with sickle cell disease in various stages of disease. Plasma samples were obtained from nineteen patients with sickle cell disease during acute chest syndrome (pre- and postexchange transfusion), vasoocclusive crisis, and/or at baseline; 12 normal volunteers served as controls. F-2 isoprostanes were measured by gas chromatography/mass spectrophotometry. There was a 9-fold increase in F-2 isoprostanes in patients with acute chest syndrome as compared with normal volunteers. There was approximately a 50-60% decline in isoprostanes postexchange transfusion to a level similar to that of patients with sickle cell disease at baseline. There was no difference in isoprostanes between vasoocclusive crisis and patients with sickle cell disease at baseline. Increased oxidative stress, measured by generation of F-2 isoprostanes, occurs during acute chest syndrome and may have an important role in the pathogenesis of this disease process.
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