Superoxide radical: A likely link between reperfusion injury and inflammation

Abstract

The roles of the superoxide free radical (0₂^.-) in the inflammatory process are known to include bactericidal action as well as participation in cell-to- cell communication via the activation of a superoxide-dependent chemo-attractant. A role for the radical is now also understood in post-ischemic injury brought about by the reintroduction of molecular oxygen. In this case the superoxide is produced within the reperfused tissue by the en~me xanthine oxidase. While the mechanisms of free radical production are biochemically distinct in these two pathological conditions, there are logical links apparent whereby an ischemia/reperfusion-induced injury would lead to inflammation, and conversely whereby an inflamed tissue could become vulnerable to ischemic injury. The occasional study notwithstanding, much evidence now supports roles for superoxide and hydrogen peroxide in reperfusion injury to the heart. In the rat and dog, xanthine oxidase appears to be the primary source of these forms of active oxygen. Manifestations of injury include inactivation of specific enzymes, functional impairment of the mitochondria, and conductance abnormalities.