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哮喘、慢性阻塞性肺疾病及吸烟者中的全身性氧化应激

Systemic oxidative stress in asthma, COPD, and smokers.

作者信息

Rahman I, Morrison D, Donaldson K, MacNee W

机构信息

Department of Medicine, University of Edinburgh, Royal Infirmary, Scotland, United Kingdom.

出版信息

Am J Respir Crit Care Med. 1996 Oct;154(4 Pt 1):1055-60. doi: 10.1164/ajrccm.154.4.8887607.

Abstract

An imbalance between oxidants and antioxidants is proposed in smokers and in patients with airways diseases. We tested this hypothesis by measuring the Trolox equivalent antioxidant capacity (TEAC) of plasma and the levels of products of lipid peroxidation as indices of overall oxidative stress. The plasma TEAC was markedly reduced (0.66 +/- 0.07 mmol/L; mean +/- SEM; n = 11), with increased levels of lipid peroxidation products, in healthy chronic smokers as compared with healthy nonsmokers (1.31 +/- 0.10 mmol/L, n = 14, p < 0.001), an effect that was exaggerated in those who had smoked 1 h before the study. Plasma TEAC was also low in patients presenting with acute exacerbations of chronic obstructive pulmonary disease (COPD) (0.46 +/- 0.10 mmol/L, n = 20, p < 0.001) or asthma (0.61 +/- 0.05 mmol/L, n = 9, p < 0.01) with increases in plasma lipid peroxidation products. There was a negative correlation between superoxide anion release by stimulated neutrophils and plasma antioxidant capacity (r = -0.73, p < 0.001) in patients with acute exacerbations of COPD. The profound decrease in TEAC was associated with a decreased plasma protein sulfhydryl concentrations in acute exacerbations of COPD but not in smokers or in asthmatic subjects. Therefore smoking, acute exacerbations of COPD, and asthma are associated with a marked oxidant/antioxidant imbalance in the blood, associated with evidence of increased oxidative stress. The decreased antioxidant capacity in plasma may result from different mechanisms in these conditions.

摘要

吸烟者和气道疾病患者体内存在氧化剂与抗氧化剂失衡的情况。我们通过测量血浆中Trolox等效抗氧化能力(TEAC)以及脂质过氧化产物水平来检验这一假设,以此作为整体氧化应激的指标。与健康非吸烟者(1.31±0.10 mmol/L,n = 14,p < 0.001)相比,健康慢性吸烟者的血浆TEAC显著降低(0.66±0.07 mmol/L;均值±标准误;n = 11),脂质过氧化产物水平升高,在研究前1小时吸烟的人群中这种效应更为明显。慢性阻塞性肺疾病(COPD)急性加重期患者(0.46±0.10 mmol/L,n = 20,p < 0.001)或哮喘患者(0.61±0.05 mmol/L,n = 9,p < 0.01)的血浆TEAC也较低,同时血浆脂质过氧化产物增加。COPD急性加重期患者中,刺激的中性粒细胞释放的超氧阴离子与血浆抗氧化能力呈负相关(r = -0.73,p < 0.001)。COPD急性加重期TEAC的显著降低与血浆蛋白巯基浓度降低有关,但吸烟者或哮喘患者中未出现这种情况。因此,吸烟、COPD急性加重期和哮喘与血液中明显的氧化剂/抗氧化剂失衡有关,伴有氧化应激增加的证据。在这些情况下,血浆抗氧化能力降低可能是由不同机制导致的。

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