Abstract
The role of oxidative stress in asthma is gaining increasing scientific attention. The hallmark of asthma is airway inflammation. Oxidative stress may initiate and augment inflammation, and may also result from inflammation. Exposure to tobacco smoke, ozone, diesel exhaust, and a variety of other pollutants generates reactive oxygen species and other oxidative stressors. Some studies suggest that asthmatics have a decreased ability to respond to oxidative stress, while others find upregulated antioxidative function. Oxidative stress may alter the Th(1)/Th(2) immune response and result in activation of NF-kbeta, a powerful inducer of pro-inflammatory genes. Genetic polymorphisms may play an important role in determining susceptibility to oxidative stress. Many therapeutic strategies to decrease oxidative stress in asthma have been suggested. Dietary changes, antioxidant vitamins, other antioxidant drugs, Ayurvedic supplements, and even radon exposure in a hot bathroom have been studied. Minimizing exposure of young children to environmental tobacco smoke remains paramount.
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