Cimetidine inhibits the formation of the reactive, toxic metabolite of isoniazid in rats but not in man

Bernhard H. Lauterburg, Elizabeth L. Todd, Charles V. Smith, Jerry R. Mitchell – 1 July 1985 – The hepatotoxicity of isoniazid in rats results from the metabolic activation of acetylhydrazine, a metabolite of isoniazid, by the cytochrome P450 monooxygenase system. Inhibition of the drugmetabolizing enzyme system with a compound suitable for clinical use such as cimetidine might therefore prevent liver injury in experimental animals and in patients on isoniazid without interfering with the antituberculous activity of the drug.

Acute and chronic changes in the microcirculation of the liver in inbred strains of mice following infection with mouse hepatitis virus type 3

Peggy J. Macphee, Vincent J. Dindzans, Lai‐Sum Fung, Gary A. Levy – 1 July 1985 – The acute and chronic effects of mouse hepatitis virus type 3 on the microcirculation of the liver in both semisusceptible C3HeB/FeJ and fully resistant A/J mice were studied. In the C3HeB/FeJ mice, abnormalities of microcirculatory flow were noted as early as 12 hr after infection and by 24 hr, localized avascular foci appeared. Disturbances were characterized by granular blood flow, sinusoidal microthrombi, distortion of sinusoids by edematous hepatocytes and necrotic lesions.

Opsonic activity of human ascitic fluid: A potentially important protective mechanism against spontaneous bacterial peritonitis

Bruce A. Runyon, Richard L. Morrissey, John C. Hoefs, Frederic A. Wyle – 1 July 1985 – The opsonic activity of 60 ascitic fluids from 47 patients was measured using a standard opsonophagocytic assay. Curve analysis of the opsonic activity compared to the ascitic fluid concentration of total protein, total hemolytic complement, C3 and C4 yielded correlation coefficients of 0.84 (p < 0.001), 0.84 (p < 0.001), 0.94 (p < 0.001) and 0.92 (p < 0.001), respectively. There appeared to be a threshold of concentration for each protein below which there was no killing of bacteria.

Hereditary chronic conjugated hyperbilirubinemia in mutant rats caused by defective hepatic anion transport

Peter L. M. Jansen, Wilbert H. Peters, Wouter H. Lamers – 1 July 1985 – A mutant rat strain is described with autosomal recessive conjugated hyperbilirubinemia. Transport of conjugated bilirubin and tetrabromosulfophthalein from liver to bile is severely impaired whereas uptake of organic anions from plasma to liver is normal. During the first 10 days of life, serum bilirubin levels are 147 ± 11 μmoles per liter with 68.7% diconjugates and 27.9% monoconjugates. In adult rats, serum bilirubin is 33 ± 8 μmoles per liter with 81.8% diconjugates and 12.1% monoconjugates vs.

Liver disease activity and hepatitis B virus replication in chronic delta antigen‐positive hepatitis B virus carriers

Stephanos J. Hadziyannis, Morris Sherman, Harvey M. Lieberman, David A. Shafritz – 1 July 1985 – Delta antigen is currently thought to reflect superinfection of the liver with a defective RNA virus (delta agent), requiring helper function from hepatitis B virus for its replication.

Time course and mechanism of alterations in proton relaxation during liver regeneration in the rat

H. Dirk Sostman, John C. Gore, M. Wayne Flye, G. Allan Johnson, Robert J. Herfkens – 1 July 1985 – We studied the proton T1 and T2, water and lipid content of regenerating rat liver from 1 to 7 days after 70% hepatectomy. Liver from normal and sham‐operated animals and splenic tissue from all animals were studied as controls. In vivo proton spectroscopy and imaging of liver was performed in a separate group of control and posthepatectomy rats. The T2 of regenerating liver, but not of sham or normal control liver, was prolonged.

Cellular theories of aging as related to the liver

J. Fred Dice – 1 May 1985 – The age‐associated decjline in function of several organs, including the liver, may be caused by mechanisms operating on the cellular level. Fibroblasts and several other cell types derived from normal individuals have limited lifespans in culture, and several abnormalities described for senescent cultured fibroblasts also apply to hepatocytes and other cell types obtained from aged organisms.

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