The use of 2-deoxy-D-glucose to assess changes in tumor target cell membranes in vitro.
Following short-term suspension culture, cells from the Balb/C sarcoma Meth A were allowed to incorporate both [14C] leucine and 2-deoxy-D-glucose-1-[3H] (2DG). The 2DG is trapped as a small anionic marker of the cytosol. Deviation from the kinetics of spontaneous efflux of the markers is interpreted as reflecting perturbation of the target cell membrane. In the presence of guinea pig complement and a rabbit antiserum to Meth A, enhanced 2DG efflux was effected in a titer comparable to that detected with a 51Cr-release assay. With a number of alloantisera and syngeneic immune sera, 2DG efflux was enhanced while 51Cr-release was unaffected. Only in the presence of syngeneic immune sera from mice bearing a low tumor mass, syngeneic splenic leukocytes effect a retardation in the spontaneous 2DG efflux. Sera from animals with a large tumor mass were ineffective. Effux of proteins labeled with [14C] leucine was not altered. The phenomenon was not dependent on the presence of a heat-inactivatable syngeneic complement source. The method described provides a sensitive probe of target cell membrane permeability in the tumor model studied. The phenomenon detected is the capacity of serum, sampled relatively early in syngeneic oncogenesis, to direct syngeneic splenic leukocytes to interact with the target cell membrane differentially altering its permeability to the small cytosol marker.
D000818:Animals; D002462:Cell Membrane / Q000276:immunology; D003165:Complement System Proteins; D003837:Deoxy Sugars / Q000378:metabolism*; D003847:Deoxyglucose / Q000378:metabolism*; D006168:Guinea Pigs; D007106:Immune Sera; D066298:In Vitro Techniques; D008748:Methylcholanthrene; D051379:Mice; D008807:Mice, Inbred BALB C; D012513:Sarcoma, Experimental / Q000139:chemically induced*; D013154:Spleen / Q000276:immunology
D003837:Deoxy Sugars; D007106:Immune Sera; D008748:Methylcholanthrene; D003165:Complement System Proteins; D003847:Deoxyglucose