Oxidative Stress in Experimental Models of Acute Lung Injury

Overproduction of oxidants within the lung leads to acute lung injury (ALI) which may progress to irreversible lung fibrosis. The sources of oxidants may be (1) intrinsic, that is, derived from phagocytic macrophages and neutrophils and endothelial and alveolar epithelial cells, or (2) extrinsic, that is, caused by inhaled pollutants or high concentrations of oxygen. The complex antioxidant system of the body includes reduction–oxidation enzymatic systems, nonenzymatic scavengers, and dietary components which balance the concentrations of both antioxidant and oxidant substances with dominance of a reducing state. However, decreasing levels of antioxidants and/or increasing levels of oxidants disturb the stability of the antioxidant–oxidant system and lead to oxidative lung injury. Several groups of therapeutic agents, including N-acetylcysteine, flavonoids, corticosteroids, phosphodiesterase inhibitors, etc., appeared to be beneficial in the treatment of various forms of experimentally induced ALI where they significantly reduced the oxidative damage. This chapter reviews the pathophysiology and mechanisms of ALI with respect to oxidative and inflammatory changes and critically evaluates perspectives of promising treatments to prevent or to minimize the oxidative changes in experimental models of ALI reflecting possibilities of their use also in the treatment of patients with acutely damaged lung.