[Pathophysiology and pharmacology of reactive oxygen species in inflammation]

Free reactive oxygen species (ROS) are generated during cell respiration and by various metabolic processes, after reoxigenation of infarctions and to a large extent by activated phagocytes. In- and extracellular physiologic radical scavengers control the multiple reactions of ROS to prevent the generation of the highly damaging hydroxyl radical (OH). ROS damage after reoxigenation of an infarct can be reduced by employing the xanthine oxidase inhibitor allopurinol. ROS generated by activated phagocytes are both defensive and noxious. ROS reduction is achieved by applying physiologic radical scavengers as the superoxide dismutase, which are of therapeutic interest for the treatment of inflammatory joint and vascular diseases and the adult respiratory distress syndrome. Known drugs e.g. benzydamine (Tantum) are increasingly recognized to act via ROS mediated mechanisms and a ROS-targeted pharmacological research appears now possible.