摘要
Asthma is a disease characterized by airway chronic inflammation and bronchial hyperactivity, involving the imbalance of oxidative and antioxidative agents. There is an increased free radical generation and a decreased antioxidant enzyme activity, which correlate with the severity of the disease. The oxidative stress triggers specific physiopathological changes in the respiratory tract as a result of proinflammatory molecule formation, such as isoprostanes and PAF- like lipids. The synthesis of these mediators is dependent on the availability of lipid substrates, such as PUFAs, which are present in cell membranes. Therefore, lipid oxidation may have an important role in the perpetuation and amplification of the asthmatic inflammatory response. This article will make considerations about how oxidative stress contributes to asthma pathogenesis.
Asthma is a disease characterized by airway chronic inflammation and bronchial hyperactivity, involving the imbalance of oxidative and antioxidative agents. There is an increased free radical generation and a decreased antioxidant enzyme activity, which correlate with the severity of the disease. The oxidative stress triggers specific physiopathological changes in the respiratory tract as a result of proinflammatory molecule formation, such as isoprostanes and PAF- like lipids. The synthesis of these mediators is dependent on the availability of lipid substrates, such as PUFAs, which are present in cell membranes. Therefore, lipid oxidation may have an important role in the perpetuation and amplification of the asthmatic inflammatory response. This article will make considerations about how oxidative stress contributes to asthma pathogenesis.
