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Electron microscopic study of Kupffer-cell phagocytosis blockade induced by gadolinium chloride.

E. Husztik, György Lázár, Á. Párducz

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Abstract

The cellular basis of Kupffer-cell phagocytosis blockade induced by gadolinium chloride was studied in rats. Investigations with heterologous erythrocytes labelled with 51Cr show that the gadolinium chloride-induced reticuloendothelial blockade is due to the depressed phagocytic activity of the Kupffer cells. Our light-microscopic studies indicate that, as a result of the action of gadolinium chloride, the impaired Kupffer-cell phagocytosis is observed not only in normal, non-activated Kupffer cells, but also in those activated with a reticuloendothelial stimulant, Zymosan. Our electron-microscopic investigations suggest that the failure of the Kupffer cells to incorporate carbon during the reticuloendothelial blockage induced by this rare earth metal chloride is due to defects in the surface attachment and in the engulfment phases of phagocytosis.

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The cellular basis of Kupffer-cell phagocytosis blockade induced by gadolinium chloride was studied in rats. Investigations with heterologous erythrocytes labelled with 51Cr show that the gadolinium chloride-induced reticuloendothelial blockade is due to the depressed phagocytic activity of the Kupffer cells. Our light-microscopic studies indicate that, as a result of the action of gadolinium chloride, the impaired Kupffer-cell phagocytosis is observed not only in normal, non-activated Kupffer cells, but also in those activated with a reticuloendothelial stimulant, Zymosan. Our electron-microscopic investigations suggest that the failure of the Kupffer cells to incorporate carbon during the reticuloendothelial blockage induced by this rare earth metal chloride is due to defects in the surface attachment and in the engulfment phases of phagocytosis.

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Available abstract

The cellular basis of Kupffer-cell phagocytosis blockade induced by gadolinium chloride was studied in rats. Investigations with heterologous erythrocytes labelled with 51Cr show that the gadolinium chloride-induced reticuloendothelial blockade is due to the depressed phagocytic activity of the Kupffer cells. Our light-microscopic studies indicate that, as a result of the action of gadolinium chloride, the impaired Kupffer-cell phagocytosis is observed not only in normal, non-activated Kupffer cells, but also in those activated with a reticuloendothelial stimulant, Zymosan. Our electron-microscopic investigations suggest that the failure of the Kupffer cells to incorporate carbon during the reticuloendothelial blockage induced by this rare earth metal chloride is due to defects in the surface attachment and in the engulfment phases of phagocytosis.

Key concepts: Phagocytosis, Mononuclear phagocyte system, Kupffer cell, Zymosan, Blockade, Chemistry, Gadolinium, Pathology

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Electron microscopic study of Kupffer-cell phagocytosis blockade induced by gadolinium chloride. — Research Paper | ScholarLens