METABOLIC CONTROL OF GLYCOLYSIS IN NORMAL AND TUMOR PERMEABILIZED CELLS

Abstract

Previous reports presented evidence suggesting the existence in tumor cells of a 2nd control site of glycolysis at pyruvate kinase and competition for ADP between this enzyme and mitochondria, which is responsible for the Crabtree effect. By using cells partially permeabilized to nucleotides and phosphorylated substrates, evidence supporting the existence in hepatocytes of partial control by ATP at phosphofructokinase, which is followed by total control by ATP at pyruvate kinase is provided. The partial or nonoperation of this 2nd site in Ehrlich ascites mouse tumor cells appears to be the cause for the characteristic aerobic glycolysis, Crabtree effect and low Pasteur effect of these cells.