Literature DB >> 2873904

Pyruvate kinase isoenzymes in altered foci and carcinoma of rat liver.

M Reinacher, E Eigenbrodt, U Gerbracht, G Zenk, I Timmermann-Trosiener, P Bentley, F Waechter, R Schulte-Hermann.   

Abstract

Pyruvate kinase (PK) isoenzymes, rate limiting for the last steps of glycolysis, were studied in normal rat liver, putative preneoplastic foci, neoplastic nodules and hepatocellular carcinoma. These lesions were produced by an initiation-promotion protocol: treatment with a single dose of N-nitrosomorpholine (NNM) was followed by feeding diets containing phenobarbital (PB) or alpha-hexachlorocyclohexane (alpha-HCH), or basal diet. PK was demonstrated (i) by immunocytochemistry on histological sections with antibodies specifically directed against the L and M2 isoenzymes, (ii) by electrophoretic separation of isoenzymes in homogenates from liver and larger tumors, and (iii) by electrophoretic separation of isoenzymes in parenchymal and stromal cells isolated from liver and tumors. Immunocytochemistry showed decreases of L-PK (L-PK-) in hepatocytes of most of the foci, nodules and carcinomas. Most L-PK- foci showed increases in gamma-glutamyltransferase (gamma-GT) and epoxide hydrolase (EH). PB or alpha-HCH treatment further decreased expression of L-PK in foci, but not in normal liver. Cells and foci with enhanced L-PK (L-PK+) were also found after carcinogen treatment. These did not show increases of gamma-GT or EH or any distinct morphological alterations with the exception of some which were basophilic ('tigroid') in H and E stained sections. No L-PK+ tumors were found. We could not demonstrate the M2-type PK in parenchymal cells of liver or any of the lesions described above. This isoenzyme was restricted to stromal cells in normal rat liver and in all stages of carcinogenesis as shown by immunohistology and by electrophoresis of preparations from isolated cell populations. However, stromal cells from hepatocellular carcinomas exhibited a 3-fold increase of M2-PK compared with stromal cells from normal liver. These results do not support an isoenzyme shift from L to M2-PK in the course of malignant transformation of hepatocytes as suggested previously.

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Year:  1986        PMID: 2873904     DOI: 10.1093/carcin/7.8.1351

Source DB:  PubMed          Journal:  Carcinogenesis        ISSN: 0143-3334            Impact factor:   4.944


  5 in total

Review 1.  Tumor promotion in the liver.

Authors:  R Schulte-Hermann
Journal:  Arch Toxicol       Date:  1985-08       Impact factor: 5.153

2.  Decrease in glucokinase and glucose-6-phosphatase and increase in hexokinase in putative preneoplastic lesions of rat liver.

Authors:  G Fischer; I Ruschenburg; E Eigenbrodt; N Katz
Journal:  J Cancer Res Clin Oncol       Date:  1987       Impact factor: 4.553

3.  Histochemical and microbiochemical demonstration of reduced pyruvate kinase activity in thioacetamide-induced neoplastic nodules of rat liver.

Authors:  F Klimek; M A Moore; E Schneider; P Bannasch
Journal:  Histochemistry       Date:  1988

Review 4.  Initiation and promotion in hepatocarcinogenesis.

Authors:  R Schulte-Hermann
Journal:  Arch Toxicol       Date:  1987       Impact factor: 5.153

5.  Response of sinusoidal mouse liver cells to choline-deficient ethionine-supplemented diet.

Authors:  Elke Ueberham; Jan Böttger; Uwe Ueberham; Jens Grosche; Rolf Gebhardt
Journal:  Comp Hepatol       Date:  2010-10-13
  5 in total

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