The involvement of reactive oxygen species (ROS) in the pathogenesis of several lung diseases/injuries has been suggested. ROS are believed primarily to be generated by leukocytes (e.g. infiltrating neutrophils) although other ROS generating systems such as the xanthine/xanthine oxidase system may also be of importance. ROS may through oxidative changes exert a number of toxic effects which have been demonstrated in many different biological systems. At limited oxidative stress events such as modification of receptor activity and signalling, as well as release of endogenous mediators of inflammation may occur. One such ROS induced event, probably of importance for several lung diseases, is arachidonic acid (AA) release and metabolism to active product(s). In the lung, the release of AA results in both vaso- and bronchoconstriction, primarily caused by thromboxane A2. The molecular events leading to oxidant induced AA release and thromboxane formation are only partially elucidated.