3-chlorotyrosine as a marker of protein damage by myeloperoxidase in tracheal aspirates from preterm infants: Association with adverse respiratory outcome
3-chlorotyrosine as a marker of protein damage by myeloperoxidase in tracheal aspirates from preterm infants: Association with adverse respiratory outcome
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DOI：
10.1203/01.pdr.0000050655.25689.ce
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发表时间：
2003-03-01
影响因子：
3.6
通讯作者：
Winterbourn, CC
中科院分区：
文献类型：
--
作者：
Buss, IH;Senthilmohan, R;Winterbourn, CC
氧化损伤与呼吸窘迫早产儿慢性肺部疾病的发展有关。然而，因果关系的直接证据有限，活性氧化剂的来源尚未确定。我们之前已经表明，气管吸入物中的蛋白质羰基水平与髓过氧化物酶呈正相关，这表明中性粒细胞氧化剂可能是这种蛋白质损伤的来源。我们通过测量来自69名出生体重婴儿的气管吸入蛋白（144个样本）中的3-氯酪氨酸（中性粒细胞氧化剂次氯酸的特异性生物标志物）来扩展这些观察结果
Oxidative injury is implicated in the development of chronic lung disease in preterm infants with respiratory distress. However, direct evidence of a causal role is limited and the source of reactive oxidants has not been identified. We have previously shown that protein carbonyl levels in tracheal aspirates correlate positively with myeloperoxidase, suggesting that neutrophil oxidants could be the source of this protein injury. We have extended these observations by measuring 3-chlorotyrosine, a specific biomarker of the neutrophil oxidant, hypochlorous acid, in tracheal aspirate proteins (144 samples) from 69 infants with birth weight