Oxygen metabolism has an important role in the pathogenesis of asthma. Reactive oxygen species (ROS) produced in the course of cellular oxidative phosphorylatiop, and by activated phagocytic cells during oxidative bursts, exceed the physiological buffering capacity and result in oxidative stress. The excessive production of ROS can damage protein, lipids, nucleic acids, and matrix components. They also serve as important intracellular signaling molecules that amplify the pulmonary inflammatory-proliferative response. Repetitive cycles of hypoxia and reoxygenation associated with changes in pulmonary perfusion are postulated to activate hypoxia-inducible factor-lα and nuclear factor-κB, two key transcription factors that are regulated by changes in cellular oxygenation and cytokine stimulation, and that in turn orchestrate the expression of a spectrum of genes critical to the persistence of asthmatic bronchoconstriction. An understanding of the complex interactions involved in these pathways might allow the development of novel therapeutic strategies for patients suffering from asthma.
|Number of pages||7|
|Journal||Journal of the Chemical Society of Pakistan|
|Publication status||Published - Jun 2008|