Veterinary MedicineBiochemistryToxicologyHepatotoxicologyRadiobiologyToxicologic PathologyChemical-induced HepatotoxicityCirrhosisHepatic NecrosisHepatic ToxicityHepatocellular NecrosisLiver DiseaseCarbon Dioxide InjuryCarbon Tetrachloride HepatotoxicityCarbon Tetrachloride ToxicityHepatocellular Liver InjuryHepatocellular ToxicityHepatotoxic MechanismsMucopolysaccharide AccumulationToxicant-induced Hepatocyte Injury
Autoradiography of mouse liver after the administration of (35)S-sodium sulphate shows transient concentration of the isotope in sinusoidal walls. This phenomenon is markedly exaggerated in the acute stages of carbon tetrachloride (CCl(4)) poisoning with radioactivity appearing over viable sinusoidal cells and extracellular necrotic spaces. This is maintained for several days and there is condensation of the isotope over prominent reticulin fibres in the centrilobular zones during the stage of recovery. Negative results are obtained if the sinusoidal cells are included in the necrotic process as induced by CCl(4) or by the local application of cold to the surface of the liver. It is concluded that liver sinusoidal cells have a capacity for mucopolysaccharide synthesis which is exaggerated following the induction of hepatocyte injury. There is also evidence for continuing synthesis of sulphated mucopolysaccharide in the cirrhotic liver in relation to fibrous trabeculae and hepatocyte degeneration.
15
Fat-storing cells (lipocytes) in human liver.
S Bronfenmajer, Fenton Schaffner, H Popper · PubMed · 1966 · 162 citations