Reactive oxygen metabolites or species refer to molecules containing an oxygen atom with a partially empty outermost electron shell, these oxygen atoms are highly reactive and result in damage to other adjacent molecules. Such metabolites include the superoxide anion radical, hydroperoxyl radical, hurdoxly radical, hydrogen peroxide and hypochlorous acid.
In parynchymal and endothelial cells xanthine oxidase is the main enzyme responsible for the generataion of free oxygen radicals, whilst in leucocytes NADPH oxidase is responsible.
Oxygen free radicals produced from xanthine oxidase have a very short half life
(seconds). Thus when the hypoxanthine substrate is exhausted generation of
free radicals by xanthine oxidase ceases. In neutrophils production of oxygen
fee radicals is unlimited provided 
is available.
Production of oxygen free radicals in ischemia-reperfusion injury has been shown using electron spin resonance spectroscopy and trapping. By products of the produciton of oxygen free radicals such as peroxidated lipids are indirect evidence of the previous production of oxygen free radicals. Changes similar to those seen in ischemia-reperfusion injury have been seen on exposure of the tissues to oxygen free radicals. Treatment of tissues with agents that limit the production of oxygen free radicals (xanthine oxidase inhibitors such as allopurinol) or that scavange generated oxygen free radicals (superoxide dimutase, catalase, taurine and dimethly sulfoxide) attenuates ischemia-reperfusion injury.
The mechanism of injury of oxygen free radicals is felt to be due to rapid
reactions of the free radicals with other molecules resulting in, DNA nicking,
lipid membrare peroxidation, crosslinking and degredation of proteins.
Radicals also result in attraction and activation of inflammatory cells and
increased expression of CD11/CD18 (
integrins) on the surface of
lecocytes, P-selectin and ICAM-1 on endothelial cells, thereby promoting
leucoctye adhesion and transmigration.