Die Wirkung von Erdalkalimetallionen auf die Hemmung des Kaliumverlustes fluoridvergifteter Erythrocyten durch Substrate und Stoffwechselgifte

Abstract

The inhibition of potassium loss of fluoride poisoned (40 mequiv/l. cell suspension) human red cells by metabolic poisons and substrates at varying Ca++-concentrations has been studied. At low calcium concentrations, fluoride produces rapid potassium loss after a lag period, whereas sodium permeability is little affected. This specific action of fluoride on potassium permeability can be almost completely prevented by the addition of cyanide, monoiodoacetic acid or adenosine. At high calcium concentrations, exceeding 0.1 mequiv/l. cell suspension, fluoride destroys the permeability barrier for both sodium and potassium ions without a preceeding lag period, which eventually leads to colloid osmotic hemolysis. This effect cannot be prevented by adenosine, monoiodoacetic acid or cyanide. It is concluded that the permeability change at high calcium concentrations is independent of the action of fluoride on cellular metabolism and is due to the formation of a calcium-fluoride-complex with ligands in the outer cell surface. On the other hand, the specific effect on potassium permeability, occuring at low Ca++-concentrations, is related to the inhibition of cellular metabolism by fluoride.