Role of TPN in Control of Glycolysis 251 



Engelhardt (1939) to explain the Pasteur effect, but un- 

 doubtedly this mechanism alone does not explain the de- 

 creased glucose consumption, which we consider a sine qua 

 non condition to define the Pasteur effect (Dixon, 1937). 



The magnitude and quality of the effect of the TPN in a 

 given preparation, or cell, would depend not only on the 

 amount of coenzyme present, but as much on the relative 

 efficiency of the enzymic reactions of the pentose cycle, in 

 strict relationship with the systems that reoxidize TPNH. All 

 these inter-related activities not only depend on the capacity 

 of each particular enzyme, but also on other parameters, such 

 as relative concentration of the substrates, presence of second 

 substrates, and general conditions such as the pH of the 

 reaction medium. The marked effect of pH in opposite 

 directions upon DPN- and TPN-lactic dehydrogenase activi- 

 ties (Fig. 11) suggests the possibility that minor changes in 

 pH may influence the overall equilibria, permitting the reduc- 

 tion of pyruvate either by DPNH or by TPNH, if the pH tends 

 to be higher or lower than neutral, respectively. 



The possibility that mechanisms involving TPN play a role 

 in the Pasteur effect should be considered. We feel that enough 

 experimental data exist to support the hypothesis that the 

 Pasteur effect is obtained through a mechanism that involves 

 a competition for inorganic phosphate of phosphate acceptors 

 (Terner, 1954; Lynen, 1955; Gatt, Krimsky and Racker, 1956; 

 Wu and Racker, 1957; Holzer, Witt and Freytag-Hilf, 1958). 

 In fact, we have seen that this mechanism operates in cells to 

 effect a balance between alternative pathways and to control 

 their reactions at different levels in relation to the conditions 

 of the surrounding medium. Even if the phosphate control is 

 very important, it seems justifiable to look for other mechan- 

 isms that may operate under certain conditions. 



Summary 



The effect of the addition of triphosphopyridine nucleotides 

 on the glycolytic activity of an enriched cell-free brain pre- 

 paration was investigated. The oxidized and the reduced 



