title: Hepatic fibrosis and iron accumulation due to endotoxin-induced haemorrhage in the gerbil.
abstract: This study reports the findings of hepatic fibrosis and the accumulation of iron in the livers of 12 gerbils. The primary lesion was a haemorrhagic necrosis of the liver that was identical to that produced experimentally in the gerbil by administration of E. coli endotoxin lipopolysaccharide. The resulting extravasation of blood caused focal histiocytic reactions. The number of lesions increased with age, eventually resulting in a micronodular cirrhosis after 9 to 12 months owing to repeated episodes of endotoxin-induced haemorrhages in the liver. The accumulation of iron occurred in perisinusoidal cells, Kupffer cells and hepatocytes. The perisinusoidal cells were responsible for the subsequent hepatic fibrosis. The fibrosis associated with this condition appears to result from iron accumulation in the liver, following haemorrhage caused by endotoxin lipopolysaccharide. The gerbil is the first recorded rodent species to develop hepatic fibrosis in response to hepatic iron overload.
authors.affiliation: MRC Toxicology Unit, MRC Laboratories, Carshalton, Surrey, U.K.
authors.forename: P
authors.initials: P
authors.lastname: Carthew
authors.forename: R E
authors.initials: RE
authors.lastname: Edwards
authors.forename: B M
authors.initials: BM
authors.lastname: Dorman
mesh_terms: D000818:Animals; D056486:Chemical and Drug Induced Liver Injury / Q000150:complications / Q000473:pathology; D004195:Disease Models, Animal; D004731:Endotoxins / Q000633:toxicity*; D004926:Escherichia coli; D005260:Female; D005849:Gerbillinae / Q000378:metabolism*; D006470:Hemorrhage / Q000209:etiology; D007501:Iron / Q000378:metabolism*; D008070:Lipopolysaccharides / Q000633:toxicity*; D008106:Liver Cirrhosis, Experimental / Q000209:etiology* / Q000378:metabolism / Q000473:pathology; D008297:Male
chemical_list: D004731:Endotoxins; D008070:Lipopolysaccharides; D007501:Iron