Hepatocellular injury inhibits lectin-mediated tumor colonization into BALB/c-mice livers.
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.
Beuth
J
J
Institute of Medical Microbiology and Hygiene, University of Cologne, Germany.
Ko
H L
HL
Steuer
M
M
Pulverer
G
G
D000818:Animals; D002252:Carbon Tetrachloride Poisoning / Q000473:pathology*; D005688:Galactosamine / Q000633:toxicity*; D008099:Liver / Q000187:drug effects / Q000473:pathology*; D008106:Liver Cirrhosis, Experimental / Q000473:pathology*; D008113:Liver Neoplasms / Q000473:pathology*; D008175:Lung Neoplasms / Q000473:pathology*; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D012513:Sarcoma, Experimental / Q000473:pathology*; D014407:Tumor Cells, Cultured
D005688:Galactosamine