Likewise, the action of such established antiflammatory drugs may be at least partiallym dependent upon interference with active oxygen metabolism in phagocytes.

Further, peroxidase release from eosinophils may playa similar role in inhibition of the inflammatory response (201) while the antioxidant properties of ceruloplasmin may also give this compound antiinflammatory properties.(21,128).

An illustrative (albeit circumstantial) model for the role of superoxide in rheumatoid arthritis can be postulated as follows: Granulocytes tend to be concentrated at sites care of active rheumatic disease, presumably in response to the presence skin spin trap of immune complexes and other immunomodulator substances. nitrone cerovive is the tradmark of the astrazeneca corporation renovis renovis

This is of some clinical importance, since an antiinflammatory pharmaceutical preparation rich in sod is used in veterinary medicine and recently has been shown to be both effective and apparently safe in the treatment of various inflammatory lesions in man. Catalase has also been used in the treatment of arthritic disease in man with reported success. (195). Superoxide, peroxide, and other active oxygen species produced further kindle the inflammatory process by specific mechanisms such as those outlined in Figure 4. Catalysis of radical oxidations by transition-sernies metals may also play a role. Agents such as ectopic SOD may interfere with this process by destroying active oxygen species or increasing peroxide fluxes, thus interfering with one or more of the mechanisms detailed above and in Figure 4.

. Both direct and indirect production of active oxygen species may also have a role in the pathophysiology of gout and other hyperuricemic syndromes.(24,26,173,138,203,204). For example, urate, a reducing agent, is present in the extracellular environment at concentrations approximating 0.3 mMolar (130). Like many reducing agents, it apparently has both antioxidative (3O-134) and autooxidative (24) properties. In fact, it may have taken over some of the functions of ascorbate in primates.(133). Likewise, xanthine oxidase is an effective producer of oxygen radical species, while urate itself stimulates the production of active species of oxygen by phagocytes (203,204) and may protect cycloepoxigenase from autooxidation.(131) The effectiveness of SOD in the treatment of urate-induced inflammatory disease in Dalmations suggests a role for superoxide in this lesion.(138).

Production of active oxygen species by activated phagocytes may also have a role in vascular (and other) damage following endotoxin shock,(144,145,205), burn-induced plasma volume loss (71) and even in atherosclerosis.(205). Similar mechanisms may account for the possible role of radical species in the progression of damage following neuronal injury.(14,17,56,171,206). Antioxidants such as the methoxyphenols are apparently effective in the amelioration of both experimental cerebral edema and spinal cord injury.(17,56). However, once again we must emphasize that, like most else in this field, the evidence for free radical involvement in inflammation and neuronal injury is circumstantial and has not been proven conclusively.

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