246 



Van R. Potter and Hermann Niemeyer 



a negligible to a significant inhibition. As occurred with 

 TPN, when TPNH alone produced an increase in glucose 

 consumption, the reverse effect was observed in the presence 

 of mitochondria. Parallel to this effect of mitochondria was 

 the conversion of TPNH into TPN, as is shown in Fig. 5. In 

 fact, only when mitochondria were present could a net and 



> 



^^^TPN 



^$:^^$j^ TPNH 



?^^$:^^;^^^^ 6 -P- GLUCONATE 



*jm ♦a lactate 



r>j> ^ gy 



pM -A GLUCOSE 

 Q ro 4^ <y) 



^^^^^NONE 



^^^^NONE 



^^^TPN 



^^^^TPNH 



^^^6-P-GLXONATE 



^^^^^^^ 



^^^^TPN 



^^ TPNH 



^^^6-P-GLXONATE 



NONE 



^^^^TPN 



^^^TPNH 



^^6-P-GLUCONATE 



Fig. 12. Effect of 6-phosphogluconate on glycolysis. The com- 

 position of the medium was as in Fig. 2, but • 1 [jlm cytochrome c 

 was added. 100 mg.-equiv. of liver mitochondria were added as 

 shown. 3 JJ.M of triphosphopyridine nucleotides or 6-phospho- 

 gluconate were added when indicated. The bars represent the 

 average of duplicate flasks for each experimental condition. 



significant production of TPN from TPNH be demonstrated. 

 This means that the effect of the TPN-lactic dehydrogenase 

 was not enough to surpass the reductive activity of the de- 

 hydrogenases of the pentose cycle that operate in the system. 

 It must be pointed out that there was not a good cor- 

 relation between the amount of the oxidized form of the co- 

 enzyme in the medium and the inhibitory effect on glycolysis, 

 either with TPN or with TPNH added initially, in the presence 



