Abstract
Fluoride, like iodoacetamide, inhibits active sodium extrusion from swine erythrocytes. The latter acts by inhibiting metabolism of adenosine (provided as a substrate) with the result that cellular ATP disappears within 2 hours. However, fluoridetreated cells contain 85% as much ATP as control cells, and P 32 incorporation into ATP is only slightly depressed. Lactic acid production is decreased by fluoride only during the early part of an experiment. Fluoride, in concentrations capable of blocking ion transport, inhibits an ATPase known to be required for this process. The data suggest that inhibition of sodium extrusion is the result of failure of this enzyme, not because ATP synthesis stops. Human erythrocytes provided with adenosine also have near normal ATP levels. Lactic production is decreased only moderately by fluoride in concentrations known to block glycolysis completely.
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