5-hydroxy-6-8-11-14-eicosatetraenoic-acid and Liver-Diseases

Arachidonate metabolism was examined in rats with experimentally induced acute and chronic liver injuries. Acute liver injury was induced by a single administration of D-galactosamine (D-Galn) and lipopolysaccharide (LPS) or carbon tetrachloride (CCl4). Chronic liver injury was produced by several administrations of CCl4 for 5 weeks. Non-parenchymal liver cells from rats with D-Galn/LPS-induced acute liver injury produced prominently leukotriene B4 and 5-hydroxy-arachidonic acid which were hardly synthesized by the normal rat liver. No apparent changes were observed in the arachidonate metabolism of the non-parenchymal cells of the acute CCl4-injured liver. In chronic liver injury, the production of 6-ketoprostaglandin F1 alpha, a stable metabolite of prostaglandin I2, by the non-parenchymal cell fraction was significantly enhanced in contrast with the fixed amount of the other arachidonate metabolites. These results suggested the arachidonate metabolism by non-parenchymal liver cells might change according to the pathogenesis of the liver disease.

Topics: Acute Disease; Animals; Arachidonic Acids; Carbon Tetrachloride; Chemical and Drug Induced Liver Injury; Chronic Disease; Eicosanoids; Galactosamine; Hydroxyeicosatetraenoic Acids; Leukotriene B4; Lipopolysaccharides; Liver; Liver Cirrhosis, Experimental; Liver Diseases; Male; Prostaglandin-Endoperoxide Synthases; Prostaglandins; Rats; Rats, Wistar