SummaryIn the present study we investigated the effects of 11 kinds of edible seaweeds (6 brown and 5 red algae) which contain characteristic seaweed dietary fibers on the induction of D -GalN ( D -galactosamine)-hepatopathy in rats (Exps. 1 and 2). Then, the efficacy of various components prepared from Gelidium sp., which was found to alleviate the hepatopathy in Exps. 1 and 2, was examined (Exp. 3). The rats were fed the diets containing various kinds of seaweeds (Exps. 1 and 2), or several components of Gelidium sp. such as total dietary fiber (TDF), soluble dietary fiber (SDF), insoluble dietary fiber (IDF) and dietary fiber-free components (DFFC) (Exp. 3), for 8 d. The rats in all experiments were injected with D -GalN (800 mg/kg body weight) intraperitoneally at the 7th day to induce liver injury and were sacrificed 24 h after the injection of D -GalN. The serum transaminase activities (ALT and AST) and lactate dehydrogenase (LDH) were determined to evaluate the levels of hepatopathy. In Exp. 3, the total GSH concentration in the liver, plasma and cecal contents and organic acid concentration in cecal contents were also evaluated. In Exps. 1 and 2, repressive effects against D -GalN-hepatopathy were shown by four seaweeds Laminaria sp., Gelidium sp., Sargassum fulvellum and Eisenia bicyclis . In Exp. 3, it was found that protective activity in Gelidium sp. against D -GalN-hepatopathy existed not only in the SDF but also in the DFFC fraction. The results in Exp. 3 also indicated that the total GSH but not organic acid concentration in the cecal contents were significantly correlated with serum AST activity, suggesting that the protective effect of Gelidium sp. on D -GalN-hepatopathy in rats is related to GSH metabolism in the intestine. Key Words seaweed, D -galactosamine, Gelidium , agar, glutathione This research was conducted for investigation of the influence of seaweeds on the development of D -galactosamine-induced hepatopathy ( D -GalN-hepatopathy) in rats. Because D -GalN-hepatopathy resembles human acute viral hepatitis histologically, D -galactosamine ( DGalN) intoxication is used as an animal model of fulminant hepatic failure ( 1 , 2 ). D -GalN is converted to UDP-D -GalN by the enzymes in the galactose metabolic pathway in the liver ( 3 ). The exhaustion of UTP caused by the UDP-D -GalN formation process is accompanied by a decrease on hepatocellular UDP, UTP, and UDP-glucose levels ( 4 -6 ). Then, D -GalN prevents the synthesis of RNA and protein in the liver, which leads to a defect in some important cell membrane proteins. Besides the above-mentioned causes, the D -GalN-induced-hepatopathy is thought to be also induced by the increase of mesentery permeability of endotoxin which is a kind of natural hepatotoxin in the intestine ( 7 , 8 ). According to previous studies, bacterial translocation in D -GalNhepatopathy was reduced by intestinal excision or use of an antibiotic which reduces intestinal bacteria in the animals before D -GalN-treatment ( 9 , 10 ). In other reports, medication with g...