Energy Metabolism and Na +,K + Redistribution in Human Erythrocytes Treated with Lipopolysaccharide Endotoxin 1

Summary

High intracellular concentrations of ATP have been observed to protect human erythrocytes against the loss of K⁺ and gain of Na⁺ induced by h-LPS. This protection was abolished by ouabain, indicating that red cells treated with h-LPS are competent for cation transport mediated by Na⁺,K⁺-dependent ATPase. In addition, the failure of h-LPS to stimulate glycolysis by fragmented erythrocytes suggests that the increased glycolytic rate of intact h-LPS-treated red cells is a secondary effect of h-LPS. Thus, the cation redistribution induced by h-LPS appears not to be due to a primary effect of h-LPS on red cell energy metabolism. Since h-LPS demonstrates neither an obvious inhibitory effect on Na⁺,K⁺-ATPase activity nor a direct stimulating effect on erythrocyte glycolysis, it is proposed that a primary action of h-LPS on human erythrocytes is to increase plasma membrane permeability toward Na⁺ and K⁺. The cation redistribution resulting from increased membrane permeability would explain the secondary increase in energy metabolism observed for the h-LPS-treated intact cells. Additional studies are now required on rapid effects of h-LPS on transmembrane fluxes of cations in intact mammalian cells, and the possible role played by such effects in the biological activation of cells by h-LPS.