[Effect of macrophage stimulators on development of selective depression of liver macrophage in vivo].

A single administration of zymosan (50 mg/kg) and chito-carboxymethylated glucan (25 mg/kg) to mice was shown to improve the selective liver macrophage depression induced by gadolinium chloride (7.5 mg/kg, intravenous administration). Both beta-1,3-glucans (ChitoCMG and CMG) studied revealed the signs of liver macrophage stimulation: increased number and phagocytic activity of liver macrophages and increased serum chitotriosidase activity.

Characterization of the novel chemically modified fungal polysaccharides as the macrophage stimulators.

By means of carboxymethylation, a novel water-soluble carboxymethyl chitin-glucan (CM-CG) was prepared from the mycelium of Aspergillus niger, and its ability to stimulate macrophages was assessed and compared to that of the previously studied carboxymethylated glucan (CMG) from the yeast Saccharomyces cerevisiae. It was demonstrated that single intraperitoneal (i.p.

Intralysosomal accumulation of gadolinium and lysosomal damage during selective depression of liver macrophages in vivo.

Kinetics of gadolinium accumulation was studied by inductively coupled plasma-emission spectroscopy after intravenous injection of this agent (7.5 mg/kg) to CBA mice. Gadolinium exhibits lysosomotropic properties (long-term selective accumulation in lysosomes in vivo).

Effect of liver macrophage depression on the development of liver metastases of HA-1 tumor in mice.

Gadolinium chloride (5 mg/kg) administered to mice 24 h before intravenous transplantation of HA-1 hepatoma cells decreased the volume density of tumor implants in the liver, reduced the intensity of degenerative and necrotic changes developing under the effect of growing tumor metastases, and prolonged the life span of tumor-bearing mice. Development of metastases was not associated with changes in cathepsin B activity in the liver, while activity of cathepsin L decreased only during the early period (4 days) after injection of gadolinium chloride. Injection of gadolinium chloride led to labilization of liver cell lysosomes because of overload with gadolinium chloride particles.