The mechanisms of glutaraldehyde-fixed sarcoma 180 ascites cell aggregation.

Abstract

Sediment height analysis was employed to investigate the mechanisms of cell aggregation by glutaraldehyde-fixed sarcoma 180 ascites cells. The aggregation of these cells proceeds by a polymer bridging mechanism in which the surface molecules of one cell associate directly with the surface molecules of adjacent cells by nonbonding interactions. The ability of adhesive surface macromolecules to serve as polymer bridges is regulated by hydrophobic and coulombic interactions. Hydrophobic interactions are not significantly involved in polymer bridging per se, but instead appear to operate either intramolecularly or between adjacent molecules of the same cell surface, and regulate the conformation and ability of such molecules to form stable intermolecular associations with the surface adhesive molecules of a nearby cell. A disruption of these intrasurface hydrophobic interactions generally promotes cell aggregation. Coulombic forces generated by the fixed charges of surface molecules inhibit aggregation; their diminution by charge neutralization promotes aggregation. It is likely that coulombic repulsive forces regulate intramolecular associations, interactions between adjacent molecules arising from the same cell surface, and interactions between macromolecules arising from different cell surfaces. The actual forces which serve to aggregate two fixed cells are not hydrophobic, but have characteristics commonly attributed to hydrogen bonding. Ion-pairing does not seem to play a role in the aggregation of fixed cells under physiological electrolyte conditions, nor does disulfide bridging.