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

被引：81

作者：

Klings, ES ^{[1
]}

Farber, HW ^{[1
]}

机构：

[1] Boston Univ, Sch Med, Ctr Pulm, Boston, MA 02118 USA

来源：

RESPIRATORY RESEARCH | 2001年 / 2卷 / 05期

关键词：

acute chest syndrome (ACS); endothelium; hemoglobin; nitric oxide (NO); oxidant stress;

D O I：

10.1186/rr70

中图分类号：

R56 [呼吸系及胸部疾病];

学科分类号：

摘要：

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.

引用

页码：280 / 285

页数：6

共 64 条

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