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Iron free radicals and arthritis

In the present review we propose that the mobile and inflamed human joint is subject to cycles of ischaemia followed by reperfusion. Ischaemic reperfusion cycles lead to iron decompartmentalization which promotes oxygen radical damage. Reactive 0 2 species have the capacity to cause damage to a variety of biomolecules in the joint, eventually leading to a persistent and locally destructive inflammatory process. Fe overload appears to selectively worsen joint inflammation whilst nutritional Fe deficiency has the converse effect. We speculate that nutritional Fe deficiency suppresses joint inflammation by reducing the activity of the enzyme xanthine oxidase (EC 1.1.3.22).