Mechanism of the linkage between te electrophoretic mobility and oxygen uptake of ascites tumor cells.

Electrophoretic mobility, glucose metabolism, and oxygen uptake were studied in three leukemic and in four nonleukemic strains of ascites tumor cells. The cells differed markedly in mobility. This variation was related neither to cell growth nor to rates of endogenous respiration and aerobic glycolysis. The nonleukemic tumor cells showed higher mobility than did the leukemic cells. Additional increases in mobility appear to be related to suppressed oxygen uptake, which results from the addition of glucose or 0.05 mM 2,4-dinitrophenol. The augmented negative surface charge does not seem to be related to those ionogenic sites susceptible to neuraminidase. However, RNase treatment of the nonleukemic tumor cell does reveal the presence in their surface membrane of negatively charged sites susceptible to this enzyme. Such RNase-susceptible ionogenic sites presumably redistribute at the cell surface membrane from the inner sites as a response to suppressed oxygen uptake. This results in a higher negative surface charge and increased mobility. The leukemic cells, on the other hand, did not show any change in oxygen uptake or mobility in the presence of glucose. Moreover, the reduced rate of oxygen uptake induced by the addition of 0.05 mM 2,4-dinitrophenol did not result in any significant alterations in mobility. This is consistent with the observation that the ionogenic sites susceptible to RNase do not appear at the surface of the leukemic cells upon suppressed oxygen uptake. The leukemic cells have thus been shown to differ from the nonleukemic tumor cells in certain aspects of their glucose metabolism as well as in the electrophoretic properties of their surface.