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A model of skin inflammation induced by reactive oxygen species has been established using the hydrogen-peroxide-producing enzyme glucose oxidase. As a means of increasing the half-life of the enzyme and tissue retention polyethylene glycol (PEG) was attached. A rapid inflammatory response occurred consisting of an oedematous, non-erythemic swelling lasting at least 48 h. Histologically, there was an infiltration of the dermis by monocytes and neutrophils, collagen matrix breakdown and damage to the vascular endothelium. This response was significantly inhibited by both catalase and superoxide dismutase attached to PEG (PEG-CAT and PEG-SOD, respectively). PEG alone produced no effects. PEG-CAT was able to sustain an inhibitory effect for at least 12 h, whereas PEG-SOD significantly reduced inflammation for up to 6 h. PEG-SOD may have an exacerbatory effect over longer periods.

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The effect of iron was studied in rats in a ROS-initiated model of acute skin inflammation. Iron dextran was administered i.v. 24 h before the induction of the inflammatory response by intradermal injection of glucose oxidase attached to polyethylene glycol (GOD-PEG). Iron exacerbated the response at 24 and 48 h (P greater than 0.001). Histologically, a similar picture was seen to that without iron except for an increase in tissue oedema and matrix destruction including the skin glands. Associated with iron loading was an increase in Perls stainable iron in the skin (P greater than 0.025) and liver (P greater than 0.001). However, skin inflammation without iron loading also increased skin iron levels (P greater than 0.025). Total serum iron was decreased in iron-loaded and GOD-PEG animals (P greater than 0.01) and the unbound iron binding capacity (UIBC) increased (P greater than 0.01).