Oxygen free radicals and their products are known to be elaborated by inflammatory cells during the 'respiratory burst'. Xanthine oxidase combined with hypoxanthine was injected into the anterior chamber of rabbit eyes. This combination is known to result in the production of oxygen free radicals. Iris fluorescein angiography performed 2 h and 24 h following injection of xanthine oxidase and hypoxanthine into the anterior chamber resulted in increased iris vascular permeability. The increased permeability was not modified by either of the prostaglandin inhibitors naproxen or aspirin nor by the free radical scavenger D-penicillamine. This study demonstrates that iris vascular permeability, and possibly blood-aqueous barrier permeability is increased following exposure to chemically generated oxygen free radicals. It is possible that the increased iris vascular permeability that occurs during ocular inflammatory processes may in part be mediated by oxygen free radical products. This model may be useful in developing therapeutic modalities directed at preventing the damaging effect of oxygen free radical products, and this may be of benefit in reducing the untoward effects of ocular inflammatory disorders.