Antioxidant Strategies in the Treatment of Bronchial Asthma

The oxidant-antioxidant hypothesis and asthma: The pathogenesis of asthma is unknown but imbalances between oxidants and antioxidants are believed to play a fundamental role. One key component of the oxidant-antioxidant hypothesis centers on the huge burden of oxidants derived from inflammatory cell infiltration into the lung. The eosinophil, in particular, is implicated as a major source of oxidative injury, including protein nitration 1. Dysfunctional mitochondria in lung cells are another potential source of oxidants. Mitochondrial injury to airway epithelium occurs in murine models of allergic asthma 2, 3. There is evidence to support its role in human asthma as well including increased oxidative injury to mitochondrial epithelial cell superoxide dismutase (SOD) 4, enhanced mitochondrial proliferation in bronchial smooth muscle 5, and mutations in mitochondrial DNA 6. Overall, this oxidative burden, generated by both inflammatory and lung cells, can overwhelm antioxidant defense to cause oxidant stress during asthma. This stress can alter or inactivate the function of essential proteins, lipids and nucleic acids culminating in severe cell injury, dysfunction and death.