ABSTRACT
According to the lungs’ physiological function for gas exchange, high oxygen partial pressures are normally present in the alveolar spaces. Consequently, the lungs are usually exposed to a higher oxidative burden than any other organ. Therefore, the lungs are equipped with a complex antioxidant defense system, which normally protects the lung from injury. However, it has also been recognized that oxygen toxicity may occur under certain circumstances. Prolonged hyperoxia (> 60%) may result in acute pulmonary edema, which is believed to be induced by formation of oxygen-derived radicals which ultimately surmount all defense mechanisms (1). In recent years, oxidative injury has been identified to contribute significantly to a number of bronchopulmonary diseases (Table 1). Oxidative pathomechanisms have been intensively studied in fibrotic lung diseases and in the clinical setting of idiopathic pulmonary fibrosis (IPF). The available evidence suggests that oxidative stress and antioxidant deficiency mutually support the evolution of the disease process in IPF. Therefore, antioxidative therapy offers a promising new treatment strategy in this usually fatal disease.
