Role of oxygen radicals on bronchial asthma.

Takao Fujisawa
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引用次数: 49

Abstract

Bronchial asthma is an inflammatory disorder characterized by recruitment and activation of various inflammatory cells including eosinophils and T cells in the airway mucosa. Oxygen radicals are produced by inflammatory cells in the airways and/or inhaled directly from environmental air. There is ample evidence that oxygen radical production is increased in asthma and is closely related to the pathogenesis and that exogenous oxidants such as cigarette smoke and ozone directly cause asthma exacerbation. The mechanism by which oxygen radicals cause asthma pathology is oxidation or nitration of proteins, lipids, or DNA to cause dysfunction of these molecules. In addition, physiological antioxidant system, which is equipped to protect host from detrimental oxidants, is impaired in asthma, possibly because of inflammation. Thus, the imbalance between oxidant and antioxidant that is called oxidant stress is critical in asthma pathogenesis. Elegant technique to measure oxygen radicals and the footprints of oxidant stress in patients with asthma have been developed and give an important clue to evaluate possible involvement of oxygen radicals in individual pathophysiology. Therapeutic interventions that reduce oxidant stress and enhance antioxidant defense may be useful in the treatment of asthma.

氧自由基在支气管哮喘中的作用。
支气管哮喘是一种炎症性疾病,其特征是气道粘膜中嗜酸性粒细胞和T细胞等多种炎症细胞的募集和激活。氧自由基是由气道中的炎症细胞和/或直接从环境空气中吸入产生的。有充分的证据表明,氧自由基的产生在哮喘中增加,并与发病机制密切相关,而香烟烟雾和臭氧等外源性氧化剂直接导致哮喘加重。氧自由基引起哮喘病理的机制是蛋白质、脂质或DNA的氧化或硝化作用,导致这些分子功能障碍。此外,保护宿主免受有害氧化剂侵害的生理抗氧化系统在哮喘中受损,可能是因为炎症。因此,被称为氧化应激的氧化剂和抗氧化剂之间的不平衡是哮喘发病的关键。测量氧自由基和哮喘患者氧化应激足迹的优雅技术已经发展起来,并为评估氧自由基在个体病理生理中的可能参与提供了重要线索。减少氧化应激和增强抗氧化防御的治疗干预措施可能有助于治疗哮喘。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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