Effects of particulate beta-1,3 glucan on human, rat, and guinea pig complement activity.

Particulate glucan, a beta-1,3-linked polyglucose derived from Saccharomyces cerevisiae, has been demonstrated to have a wide range of immunopotentiating effects. Glucan administration is associated with the modification of a variety of experimentally induced infectious disease states as well as the inhibition of growth of implantable and spontaneous tumors. The present study was designed to evaluate the effect of glucan upon activation of the complement system in rats and guinea pigs.

Quantitative requirements for C3 to induce Forssman systemic shock and cutaneous hemorrhagic vasculitis in guinea pigs.

The requirements of complement (C) to induce systemic and cutaneous Forssman reactions were studied in inbred DHC-BA and Hartley strain guinea pigs. After intravenous injection of Forssman antibody, fatal systemic shock was associated with a marked drop in CH50, C4, and C3 and a lesser decrease in C5 hemolytic activity. Platelet counts and leukocyte counts dropped as well.

Hypersensitivity to procarbazine associated with angioedema, urticaria, and low serum complement activity.

Hypersensitivity to procarbazine associated with urticaria, angioedema, and painful joint swelling was found in a 20-year-old student being treated for Hodgkin's disease. A marked fall in complement component activity occurred simultaneously with the development of symtoms. It is suggested that generation of products of complement component activation could be important in the pathogenesis of hypersensitivity to some drugs.

Inhibition of guinea-pig complement by derivatives of benzamidine. I. Effect of p-nitrophenylureido derivative of m-(m-phenoxypropoxy)benzamidine on guinea-pig complement component haemolytic activity.

Derivatives of benzamidine have been shown to be potent inhibitors of whole guinea-pig complement. Among these compounds the -[-(-nitrophenylureido) phenoxypropoxy] benzamidine (NPUPPB) was the most potent complement inhibitor synthesized. NPUPPB blocked the addition of C1 to EAC4.