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Nonimmunologic Complement Activation in Normal Human Serum Induced by Radiographic Contrast Media¹

From the Department of Molecular Immunology, Scripps Clinic and Research Foundation, La Jolla, California 92037 and the Department of Radiology, School of Medicine, University of California at San Diego, La Jolla, California 92037

Abstract

Two different radiographic contrast media (RCM), iothalamate and iodipamide, induced the activation of several complement (C) components in normal, genetically C2-deficient and agammaglobulinemic human sera in vitro. This activation was dose dependent and demonstrable by a reduction in whole C as well as C4, C2, C3, and C5 hemolytic activities. C6, C8, and C9 hemolytic activities were unaffected. Concommitant with the loss of C3 hemolytic activity was the appearance of C3 proteolytic cleavage products that were identified by immunoelectrophoresis. Both the loss of C3 hemolytic activity and the production of C3 fragments occurred in the presence of 10 mM EDTA, indicating RCM-induced C3 cleavage occurred without participation of the multicomponent C3/C5 convertases of either the classical or alternative C pathways. Furthermore, loss of C3 hemolytic activity was not due to the direct alteration of the C3 molecule by RCM because purified C3 was unaffected upon incubation with RCM at a concentration that induced 80% reduction in the C3 hemolytic activity in normal human serum.

Serum samples obtained from 40 patients, before and 30 min after undergoing i.v. pyelography, revealed no significant change in total hemolytic C activity; 34 patients received sodium and methylglucamine diatrizoate and six received sodium iothalamate. Hemolytic C3 levels were also determined for the six patients before and 30 min after administration of sodium iothalamate and no significant change in activity was detectable.

Footnotes

¹ This is publication Number 1138 from Scripps Clinic and Research Foundation. Supported by United States Public Health Service Grants GM 16593 and A1 07007 from the National Institutes of Health.

² Dr. Kolb is the recipient of Research Career Development Award No. 7 KO4 CA 00412. Address reprint request to: William P. Kolb, Department of Biochemistry, University of Texas Health Science Center, San Antonio, Texas 78284.