Evidence for a role of hydroxyl radical in immune-complex-induced vasculitis.

摘要: Previously it was shown that tissue injury occurring in acute immune-complex-induced vasculitis, which is complement and neutrophil-dependent, significantly attenuated by the presence of catalase, suggesting pathogenic role H2O2 generated from activated neutrophils. We now show significant protection also afforded pretreatment animals with apolactoferrin , a naturally chelator iron. Iron-saturated lactoferrin devoid protective effects. Deferoxamine mesylate, synthetic iron chelator, has Infusion ionic iron, especially Fe(III), potentiates injury. Significant produced treatment rats dimethyl sulfoxide, potent hydroxyl radical scavenger. Morphologically, treated these interventions influx neutrophils into sites immune complex deposition, but there markedly edema, little or no hemorrhage, evidence endothelial cell injury, contrast to findings nonprotected animals. These data support suggestion may be linked generation subsequent conversion radical.