Oxidative Damage and Bronchial Asthma

All organisms live in the environment that contains oxygen which is vital for all aerobic organisms, and reactive oxygen species (ROS) which are formed in cells as a consequence of aerobic metabolism. Moreover mitochondrial respiration (a base of energetic production in all eukaryotic organisms) is associated with an inevitable electron leak, resulting in a nonstop production of reactive oxygen species, such as superoxide anion radical, hydrogen peroxide and hydrogen radical. Universal nature of reactive oxygen species is underlined by the presence of one enzyme superoxide dismutase. This enzyme occurs in all aerobic organisms and it is responsible for dismutation of superoxide anions into oxygen and hydrogen peroxide. Genes involved in detoxification of reactive oxygen species are highly conserved among eukaryotes and their deficiency could be limit of several diseases and life span. Oxidative stress is a unique pathophysiological condition resulting from the disrupted balance between oxidants and antioxidants. Increased level of reactive oxygen species may cause oxidative damage of all biomolecules: nucleic acids, proteins, lipids, saccharides. A progressive grow of oxidative damage is the result of increasing production of reactive oxygen species or an insufficient antioxidant defence system and this damage may contribute to the origin and development of several diseases including bronchial asthma, but on the other hand oxidative damage can be the consequence of them as well (fig. 1).