EVIDENCE FOR A ROLE OF HYDROXYL RADICAL IN IMMUNE-COMPLEX-INDUCED VASCULITIS

  • 1 January 1984
    • journal article
    • research article
    • Vol. 115  (3) , 375-382
Abstract
Tissue injury occurring in acute immune-complex-induced vasculitis, which is complement and neutrophil-dependent, is significantly attenuated by the presence of catalase, suggesting the pathogenic role of H2O2 generated from activated neutrophils. Significant protection is also afforded by pretreatment of animals with apolactoferrin, a naturally occurring chelator of Fe. Fe-saturated lactoferrin is devoid of protective effects. Deferoxamine mesylate, a synthetic Fe chelator, also has protective effects. Infusion of ionic Fe, especially Fe(III), potentiates the tissue injury. Significant protection from tissue injury is also produced by treatment of rats with dimethyl sulfoxide, a potent hydroxyl radical scavenger. Morphologically, animals treated with these protective interventions show the influx of neutrophils into sites of immune complex deposition, but there is markedly attenuated edema, little or no hemorrhage and litte evidence of endothelial cell injury, in contrast to the findings in nonprotected animals. Immune-complex-induced injury may be linked to generation of H2O2 from activated neutrophils and the subsequent conversion of H2O2 to the hydroxyl radical.