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Hepatocellular injury inhibits lectin-mediated tumor colonization into BALB/c-mice livers

Experientia volume 49, pages 547–550 (1993)Cite this article

Abstract

Acute (hepatitis) and chronic (cirrhosis) liver injuries were experimentally induced in BALB/c-mice by administration of D-galactosamine and carbon tetrachloride, respectively. In both experimental liver diseases the incidence of hepatic tumor colonization of sarcoma L-1 was significantly reduced as compared to non-treated control animals. Thus, it seems that either dysfunction or loss of organ-characteristic lectins (galactosyl-specific hepatic lectins) prevented liver colonization. Histochemical staining of liver sections from D-galactosamine or carbon tetrachloride-treated mice with appropriate galactose-containing (neo) glycoproteins supported this hypothesis, since the lectin-dependent binding was greatly reduced as compared to sections from non-treated animals.

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Affiliations

  1. Institute of Medical Microbiology and Hygiene, University of Cologne, Goldenfelsstraße 19-21, 5000, Cologne 41, (Germany)

    J. Beuth, H. L. Ko, M. Steuer & G. Pulverer

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  1. J. Beuth
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  2. H. L. Ko
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  3. M. Steuer
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  4. G. Pulverer
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Beuth, J., Ko, H.L., Steuer, M. et al. Hepatocellular injury inhibits lectin-mediated tumor colonization into BALB/c-mice livers. Experientia 49, 547–550 (1993). https://doi.org/10.1007/BF01955160

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  • DOI: https://doi.org/10.1007/BF01955160

Key words

  • BALB/c-mice
  • liver cirrhosis
  • acute hepatitis
  • liver lectins
  • metastasis formation