Serum proteins in mink with endotoxin-induced amyloidosis and infectious plasmacytosis.

The serum proteins in Sapphire mink from the experimental and control groups in 2 endotoxin experiments and in a group of normal mink of the Standard type, were separated electrophoretically on cellulose acetate membranes.In experiment No. 1, in which the experimental mink were given repeated injections of endotoxin, and the controls were untreated, significantly increased total protein and significantly decreased albumin concentrations in the experimental group compared to the normal group were demonstrated. The concentration of the alpha₁-globulin was significantly elevated and the alpha₂-globulin significantly reduced in the experimental and the control groups compared to the normal group. Significant differences between the gamma-globulin concentrations in the various groups were not found.In experiment No. 2, all the animals were inoculated intraperitoneally with a crude tissue suspension containing the plasmacytosis agent 10 days before the experimental animals received the first of a series of injections with endotoxin. Significantly increased concentrations of total protein and gamma-globulin and significantly decreased albumin concentrations were, compared with the normal group, demonstrated in sera collected from the experimental group on the 94th, 201st and 254th day after the first injection of endotoxin. In the control group, compared with the normal group, significantly elevated concentrations of total protein, alpha₂-, beta- and gamma-globulins and significantly reduced albumin- and alpha₁-globulin were found but only in the second set of samples, while significantly decreased albumin- and significantly increased gamma-globulin concentrations were found in the third set.The results showed no significant differences between the gammaglobulin concentrations or between the other serum fractions in the experimental and the control groups in the 2 experiments. A possible explanation may be that there is no direct interrelationship between hypergammaglobulinaemia and amyloidosis, and that a common basic mechanism may stimulate related stem cells which thereafter differentiate in different ways.