Agglutination kinetics of enzymatically treated normal and diabetic rat hepatocytes.
The effect of trypsin and neuraminidase treatments on concanavalin A-induced agglutination of viable hepatocytes from normal and diabetic rats are reported. Trypsin (1.0 microgram/mL) treatment resulted in a increased rate of hepatocyte agglutination in both normal and diabetic cells in the presence of 100 micrograms/mL of concanavalin A. However, neuraminidase treatment resulted in a decrease in the rate of cytoagglutination in the normal cells and an increase in the rate in the diabetic counterpart. The results suggest that trypsin may have caused the removal of a surface protein and/or split a peptide bond on the agglutinin receptors resulting in identical receptor exposure and clustering in normal and diabetic cells. The neuraminidase data suggest that the arrangements of the neuraminic acid moieties on the receptors in normal cell membranes were different from those in the diabetic cells, eliminating the possible effect of changes in the surface charge density. In conclusion, normal cells carry numerous clustered (possibly some in the "cryptic" state) agglutinin receptors in the cell membrane as compared with cells from diabetic rats.
D000371:Agglutination / Q000187:drug effects; D000818:Animals; D002452:Cell Count; D002470:Cell Survival; D003208:Concanavalin A / Q000494:pharmacology; D003921:Diabetes Mellitus, Experimental / Q000378:metabolism / Q000473:pathology*; D007700:Kinetics; D008099:Liver / Q000166:cytology*; D009439:Neuraminidase / Q000494:pharmacology; D010447:Peptide Hydrolases / Q000494:pharmacology*; D051381:Rats; D014357:Trypsin / Q000494:pharmacology; D014361:Trypsin Inhibitors / Q000494:pharmacology
D014361:Trypsin Inhibitors; D003208:Concanavalin A; D009439:Neuraminidase; D010447:Peptide Hydrolases; D014357:Trypsin