Abstract
We investigated the influence of CIM and HIS on the SUP and CH in the SUP generating cell-free xanthine oxidase system and in human neutrophils. As measured by CCR or CH, we found that HIS inhibited SUP output in both systems. The HIS concentration required for a measurable inhibition was somewhat higher in the xanthine oxidase system than in neutrophils. CIM increased CH in neutrophils significantly. A similar effect of CIM was not observed in the xanthine oxidase system. CIM antagonized in neutrophils the effect of HIS. However, a five or ten times higher molar concentration of CIM than of HIS was necessary to produce this effect. The antagonistic effect of CIM was not found in the xanthine oxidase system within the concentrations applied. In addition to an interaction of HIS with neutrophils on the cellular level, we suggest a superoxidase scavenging effect caused by HIS. At the present no suggestions can be made regarding the observed SUP output stimulating activity of CIM.