Human polymorphonuclear leukocytes (PMN) had higher 67Ga uptake than lymphocytes, but red blood cells had no affinity for 67Ga. Uptake by PMN showed temperature dependence, was independent of 67Ga concentrations and was not inhibited by metabolic inhibitors. Its binding to PMN could be removed by trypsin but not by neuraminidase. These results are consistent with the hypothesis that the plasma membrane serves as a diffusion barrier and 67Ga only binds to the surface of the PMN plasma membrane. When this membrane''s permeability barrier was disrupted, as in heat-killed PMN, 67Ga uptake increased markedly. Experimental abscesses were induced with Escherichia coli or turpentine in rabbits. Twenty-four hours after i.v. injection, only 20% of 67Ga in abscesses was in fractions containing intact PMN, cell debris or bacteria; the remainder was in a soluble, non-cellular fraction (2500-g supernatant).