CONTROL OF LACTATE PRODUCTION BY MEMBRANE ADENOSINE TRIPHOSPHATASE ACTIVITY IN HUMAN ERYTHROCYTES.

Abstract

IT is generally believed from Schatzmann's1 work that lactate production in human erythrocytes is unaffected by ouabain and other cardiac glycosides which inhibit the active transport of sodium and potassium. The absence of a direct effect on energy production was further suggested by later studies on ion movements2,3. It has thus appeared that inhibition of active transport is unaccompanied by a change in energy production in spite of the smaller energy requirements of the cell. Active transport involves the hydrolysis of ATP to ADP, and in respiring cells such as those of brain and kidney cortex, cessation of transport elicits a fall in oxygen consumption due to the decreased adenosine triphosphatase activity of the membranes4,5. Since energy production and utilization are interdependent in respiring cells, a re-investigation has been made of lactate production in the non-respiring erythrocyte to see whether the same principle also applies. In checking lactate production we have avoided Schatzmann's method of measuring the liberation of carbon dioxide from bicarbonate, during glucose metabolism by cells previously treated with carbon monoxide, and have specifically determined lactate. Moreover, our incubation conditions were the same as those employed for concomitant studies on ion movements. Lactate was measured in three ways: (a) by Hullin and Noble's modification6 of the chemical method of Barker and Summerson7; (b) by the enzymatic method of Krebs, Bennett, Gasquet, Gascoyne and Yoshida8; (c) by the method of Hohorst, Kreutz and Bucher9. Agreement was obtained among these methods.