Evaluation of cellular and humoral mechanisms of carbaryl-induced reticuloendothelial phagocytic depression.

Abstract

The simultaneous injection of carbaryl and colloidal carbon phagocytized by the reticuloendothelial cells results in competition between the two substances in favor of the carbon particles. Experiments with opsonized carbaryl suggest that the decrease in carbaryl blood clearance by the colloid is mediated by a depletion of serum opsonins. Following blockade, the liver carbaryl uptake was depressed in the control group (17%), while it was increased in the opsonized group (12%). With all preparations of carbaryl, opsonized or non-opsonized, colloidal carbon produced a slight and variable increase in carbaryl uptake by the spleen and lungs. These results indicate that, besides the uptake of carbaryl by the hepatocytes, other clearance sites must also be considered such as the Kupffer cells and other liver sinusoidal cells. Moreover our results show that intravenous administration of carbaryl induces a state of phagocytic depression as indicated by impaired intravascular phagocytosis and depressed hepatic uptake of the reticuloendothelial (RE)-test colloidal suspension. The results obtained from injection of opsonized colloidal particles during carbaryl-induced RE-depression, and the fact that carbaryl and carbon are both opsonized by the same serum factor, suggest that the mechanisms of RE-blockade involve selective hepatic and splenic macrophage failure and depletion of serum opsonins. According to our enzymatic investigation, this failure of the RE system to incorporate colloids during carbaryl--RE-blockade could be due to a defect in the activity of macrophage membrane-bound serine esterase.