Nobuyoshi Yokoe

Lipid peroxidation and lysosomal enzymes in D-galactosamine hepatitis and its protection by vitamin E

SummaryRole of Iipid peroxidation on lysosomal instability in liver tissue was investigated in an experimental model of D-galactosamine hepatitis in rats fed on vitamin E (V.E) deficient diet.Administration of D-galactisamine to V.E deficient rats resulted in a sudden increase of serum glutamic oxaloacetic transaminase (sGOT), glutamic pyruvic transaminase (sGPT), lipid peroxide value, as well asβ glucuronidase and acid phosphatase activity examined as markers of lysosomal enzymes, when compared with control rats fed on V.E supplemented diet.Lipid peroxide in the liver tissue also showed significant increase in V.E deficient rats. In contrast, \- glucuronidase and acid phosphatase in the liver tissue were found to decrease in V.E deficient rats by the administration of D-galactosamine, indicating that the enzymes in the lysosome were entirely released outside the liver cells as a result of cell destruction.It is concluded that the increase of lipid peroxide causes the instability of lysosomal membranes and releases various kinds of hydrolytic enzymes to lead further cell damage. V.E might act on inhibiting lipid peroxidation to stabilize lysosomal membranes.

Hemorrhagic Necrosis of the Intestinal Mucosa Associated with Disseminated Intravascular Coagulation

Disseminated intravascular coagulation (DIC), experimentally induced by endotoxin, caused severe hemorrhagic necrosis of the intestinal mucosa in dogs. Microscopic observation showed tortuous thrombus formation in the microcirculation of the villi. Ligation of the pancreatic and bile ducts, or administration of heparin protected the mucosa from hemorrhagic necrosis, while systemic administration of tranexamic acid increased the intestinal mucosal lesion. Local pretreatment of the intestinal mucosa by Trasylol or tranexamic acid reduced the degree of hemorrhagic necrosis. It is concluded that intravascular coagulation in the microcirculation of the intestinal mucosa, as well as pancreatic proteases, play a role in the pathogenesis of hemorrhagic necrosis in the intestine associated with DIC.

Effect of a protein-bound polysaccharide PS-K on the complement system

SummaryA protein-bound polysaccharide from mycelia ofCoriolus versicolor PS-K, clinically used as an immunomodulator, has been shown to restore the decreased cellular immune response and to exhibit host-mediated antitumor activity. In this experiment, PS-K was found to increase serum complement level in guinea pig and in human without malignancy, when hemolytic assay of complement was performed using sensitized sheep erythrocytes for the classical pathway activity and unsensitized rabbit erythrocytes for the alternative pathway activity. Assay of complement components revealed increase in C3 level in guinea pig, but no significant changes in Clq, C4, C3, properdin, C3 activator, and C

Activation of the complement by immunostimulants, BCG, OK-432 (Picibanil), and PS-K (Krestin) in vitro.

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Immune responses to an oral administration of OK-432 in the aged subjects without malignancy

-inhibitor in human, while C5 and C9 were depressed. Conversion ofβ1C toβ1A was observed in the 7th days plasma of these patients by crossed immunoelectrophoresis. Biosynthesis of guinea pig C3 was accelerated by administration of PS-K, but that of C4 was not affected. These evidences suggested that PS-K might potentiate immune response of the host by elevating serum complement level, in addition to the activation of the complement system.