In vitro binding of 67Ga to Ehrlich ascites tumor cells.
The binding of 67Ga to Ehrlich ascites tumor cells (ETC) was studied in vitro. Acid mucopolysaccharide (AMPS) present at the cell surface of ETC was identified as heparan sulfate (HS). The extent of 67Ga binding to ETC reached a plateau (ca. 10% of the added dose) at 1-2 h after the start of incubation. The binding was higher under neutral or alkaline conditions than under acidic conditions. Heparin and heparitinase treatment both significantly decreased the extent of 67Ga binding to ETC. Mild treatment with protease, including trypsin or papain, also decreased the binding. On the contrary, the treatment with trypsin under severe conditions markedly increased the extent of 67Ga binding to ETC. These results support the hypothesis that HS plays an important role as a 67Ga receptor in the mechanism of gallium binding to ETC.
D000818:Animals; D001665:Binding Sites / Q000187:drug effects; D002286:Carcinoma, Ehrlich Tumor / Q000378:metabolism*; D005710:Gallium Radioisotopes / Q000378:metabolism*; D006493:Heparin / Q000494:pharmacology; D006497:Heparan Sulfate / Q000378:metabolism; D051379:Mice; D010447:Peptide Hydrolases / Q000494:pharmacology; D011133:Polysaccharide-Lyases / Q000494:pharmacology
D005710:Gallium Radioisotopes; D006493:Heparin; D006497:Heparan Sulfate; D010447:Peptide Hydrolases; D011133:Polysaccharide-Lyases