Sodium azide inhibition of complement-mediated functions.
Moderate concentrations of sodium azide (0.1-0.2%) significantly inhibited guinea-pig and human complement-mediated lysis of both IgM- and IgG-sensitized sheep erythrocytes. The reduction in cytolysis was not attributable to non-specific ionic effects, to inactivation of native complement components by azide, or to irreversible interactions of azide with sensitized erythrocytes. Mouse complement-dependent opsonization of sensitized erythrocytes, as judged by macrophage complement receptor-mediated attachment and phagocytosis of the erythrocytes, was comparably inhibited by sodium azide, suggesting that azide acted within the sequence of the first four components of the classical complement pathway.
D000818:Animals; D001386:Azides / Q000494:pharmacology*; D003169:Complement Inactivator Proteins; D006168:Guinea Pigs; D006461:Hemolysis / Q000187:drug effects*; D006801:Humans; D007075:Immunoglobulin M / Q000276:immunology; D066298:In Vitro Techniques; D008264:Macrophages / Q000276:immunology; D009895:Opsonin Proteins / Q000276:immunology; D011951:Receptors, Complement
D001386:Azides; D003169:Complement Inactivator Proteins; D007075:Immunoglobulin M; D009895:Opsonin Proteins; D011951:Receptors, Complement